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Surgery_Schwartz. these large-bore tubes stent open the gastroesophageal junction, creating the possibility of gas-tric reflux. The use of enteric and gastric feeding tubes obviates Brunicardi_Ch12_p0397-p0432.indd 42620/02/19 3:57 PM 427QUALITY, PATIENT SAFETY, ASSESSMENTS OF CARE, AND COMPLICATIONSCHAPTER 12complications of TPN, such as pneumothorax, line sepsis, upper extremity DVT, and the related expense. There is growing evi-dence to support the initiation of enteral feeding in the early postoperative period, before the return of bowel function, where it is usually well tolerated.In patients who have had any type of nasal intubation who are having high, unexplained fevers, sinusitis must be enter-tained as a diagnosis. CT scan of the sinuses is warranted, fol-lowed by aspiration of sinus contents so the organism(s) are appropriately treated.Patients who have not been enterally fed for prolonged periods secondary to multiple operations, those who have had enteral feeds interrupted for any


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Surgery_Schwartz. so the organism(s) are appropriately treated.Patients who have not been enterally fed for prolonged periods secondary to multiple operations, those who have had enteral feeds interrupted for any other reason, or those with poor enteral access are at risk for the refeeding syndrome, which is characterized by severe hypophosphatemia and respiratory fail-ure. Slow progression of the enteral feeding administration rate can avoid this complication.Common TPN problems are mostly related to electrolyte abnormalities that may develop. These electrolyte errors include deficits or excesses in sodium, potassium, calcium, magnesium, and phosphate. Acid-base abnormalities can also occur with the improper administration of acetate or bicarbonate solutions.The most common cause for hypernatremia in hospitalized patients is under-resuscitation, and, conversely, hyponatremia is most often caused by fluid overload. Treatment for hyponatre-mia is fluid restriction in mild or moderate cases and the


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Surgery_Schwartz. hospitalized patients is under-resuscitation, and, conversely, hyponatremia is most often caused by fluid overload. Treatment for hyponatre-mia is fluid restriction in mild or moderate cases and the admin-istration of hypertonic saline for severe cases. An overly rapid correction of the sodium abnormality may result in central pon-tine myelinolysis, which results in a severe neurologic deficit. Treatment for hyponatremic patients includes fluid restriction to correct the free water deficit by 50% in the first 24 hours. An overcorrection of hyponatremia can result in severe cerebral edema, a neurologic deficit, or seizures.Glycemic Control. In 2001, Van den Berghe and colleagues demonstrated that tight glycemic control by insulin infusion is associated with a 50% reduction in mortality in the critical care setting.136 This prospective, randomized, controlled trial of 1500 patients had two study arms: the intensive-control arm, where the serum glucose was maintained between 80 and 110


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Surgery_Schwartz. the critical care setting.136 This prospective, randomized, controlled trial of 1500 patients had two study arms: the intensive-control arm, where the serum glucose was maintained between 80 and 110 mg/dL with insulin infusion; and the control arm, where patients received an insulin infusion only if blood glucose was greater than 215 mg/dL, but serum glucose was then maintained at 180 to 200 mg/dL.The tight glycemic control group had an average serum glucose level of 103 mg/dL, and the average glucose level in the control group was 153 mg/dL. Hypoglycemic episodes (glu-cose <40 mg/dL) occurred in 39 patients in the tightly controlled group, while the control group had episodes in six patients. The overall mortality was reduced from 8% to 4.6%, but the mortal-ity of those patients whose ICU stay lasted longer than 5 days was reduced from 20% to 10%. Secondary findings included an improvement in overall morbidity, a decreased percentage of ventilator days, less renal impairment, and a


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Surgery_Schwartz. stay lasted longer than 5 days was reduced from 20% to 10%. Secondary findings included an improvement in overall morbidity, a decreased percentage of ventilator days, less renal impairment, and a lower incidence of bloodstream infections. These finding have been corrobo-rated by subsequent similar studies, and the principal benefit appears to be a greatly reduced incidence of nosocomial infec-tions and sepsis. It is not known whether the benefits are due to strict euglycemia, to the anabolic properties of insulin, or both, but the maintenance of strict euglycemia between 140 and 180 mg/dL appears to be a powerful therapeutic strategy.136-138 A number of studies followed this sentinel publication of tight glycemic control. The NICE-SUGAR139 and COIITSS140 trials revisited the Van den Berghe study and found that the glyce-mic goals found initially to improve outcomes in critically ill patients were now found to be associated with a higher mortality when glucose was kept below 180


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Surgery_Schwartz. Berghe study and found that the glyce-mic goals found initially to improve outcomes in critically ill patients were now found to be associated with a higher mortality when glucose was kept below 180 mg/dL, due to an increase in incidents of hypoglycemia. When targeted goals of 180 mg/dL are achieved, fewer occurrences of hypoglycemia have been docu-mented, and improved survivorship has been achieved. In addi-tion, some studies find no relationship between glycemic control and improved outcomes. Thus, glycemic control in the critically ill still remains unclear and elusive at best.141,142 Part of the dif-ficulty in achieving “tight glycemic control” is the necessity for frequent (every 1–2 hours) blood glucose determinations. When this is performed, glycemic control is enhanced and hypoglyce-mia is avoided.Metabolism-Related Complications. “Stress dose steroids” have been advocated for the perioperative treatment of patients on corticosteroid therapy, but recent studies strongly


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Surgery_Schwartz. is avoided.Metabolism-Related Complications. “Stress dose steroids” have been advocated for the perioperative treatment of patients on corticosteroid therapy, but recent studies strongly discour-age the use of supraphysiologic doses of steroids when patients are on low or maintenance doses (e.g., 5–15 mg) of prednisone daily. Parenteral glucocorticoid treatment need only replicate physiologic replacement steroids in the perioperative period. When patients are on steroid replacement doses equal to or greater than 20 mg per day of prednisone, it may be appropriate to administer additional glucocorticoid doses for no more than 2 perioperative days.143-145Adrenal insufficiency may be present in patients with a baseline serum cortisol less than 20 μg/dL. A rapid provocative test with synthetic adrenocorticotropic hormone may confirm the diagnosis. After a baseline serum cortisol level is drawn, 250 μg of cosyntropin is administered. At exactly 30 and 60 minutes follow-ing the dose of


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Surgery_Schwartz. adrenocorticotropic hormone may confirm the diagnosis. After a baseline serum cortisol level is drawn, 250 μg of cosyntropin is administered. At exactly 30 and 60 minutes follow-ing the dose of cosyntropin, serum cortisol levels are obtained. There should be an incremental increase in the cortisol level of between 7 and 10 μg/dL for each half hour. If the patient is below these levels, a diagnosis of adrenal insufficiency is made, and glucocorticoid and mineralocorticoid administration is then warranted. Mixed results are common, but the complication of performing major surgery on an adrenally insufficient patient is sudden or profound hypotension that is not responsive to fluid resuscitation.131Thyroid hormone abnormalities usually consist of previ-ously undiagnosed thyroid abnormalities. Hypothyroidism and the so-called sick-euthyroid syndrome are more commonly recognized in the critical care setting. When surgical patients are not progressing satisfactorily in the perioperative


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Surgery_Schwartz. Hypothyroidism and the so-called sick-euthyroid syndrome are more commonly recognized in the critical care setting. When surgical patients are not progressing satisfactorily in the perioperative period, screening for thyroid abnormalities should be performed. If the results show mild to moderate hypothyroidism, then thyroid replacement should begin immediately, and thyroid function studies should be monitored closely. All patients should be reas-sessed after the acute illness has subsided regarding the need for chronic thyroid replacement therapy.Problems with ThermoregulationHypothermia. Hypothermia is defined as a core tempera-ture less than 35°C (95°F) and is divided into subsets of mild (35°C–32°C [95°F–89.6°F]), moderate (32°C–28°C [89.6°F –82.4°F]), and severe (<28°C [<82.4°F]) hypothermia. Shiver-ing, the body’s attempt to reverse the effects of hypothermia, occurs between 37°C and 31°C (98.6°F and 87.8°F), but ceases at temperatures below 31°C (87.8°F). Patients who are


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Surgery_Schwartz. hypothermia. Shiver-ing, the body’s attempt to reverse the effects of hypothermia, occurs between 37°C and 31°C (98.6°F and 87.8°F), but ceases at temperatures below 31°C (87.8°F). Patients who are moder-ately hypothermic are at higher risk for complications than are those who are more profoundly hypothermic.Brunicardi_Ch12_p0397-p0432.indd 42720/02/19 3:57 PM 428BASIC CONSIDERATIONSPART IHypothermia creates a coagulopathy that is related to platelet and clotting cascade enzyme dysfunction. This triad of metabolic acidosis, coagulopathy, and hypothermia is com-monly found in long operative cases and in patients with blood dyscrasias. The enzymes that contribute to the clotting cascade and platelet activity are most efficient at normal body tempera-tures; therefore, all measures must be used to reduce heat loss intraoperatively.146The most common cardiac abnormality is the develop-ment of arrhythmias when body temperature drops below 35°C (95°F). Bradycardia occurs with


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Surgery_Schwartz. must be used to reduce heat loss intraoperatively.146The most common cardiac abnormality is the develop-ment of arrhythmias when body temperature drops below 35°C (95°F). Bradycardia occurs with temperatures below 30°C (86°F). It is well known that hypothermia may induce CO2 retention, resulting in respiratory acidosis. Renal dysfunction of hypothermia manifests itself as a paradoxic polyuria and is related to an increased glomerular filtration rate, as peripheral vascular constriction creates central shunting of blood. This is potentially perplexing in patients who are undergoing resuscita-tion for hemodynamic instability because the brisk urine output provides a false sense of an adequate intravascular fluid volume.Induced peripheral hypothermia for hyperpyrexia due to infection (not to include neurologic or cardiac disease) is likely deleterious and does not appear to be beneficial. Plac-ing cooling blankets on or under the patient or ice packs in the axillae or groin may be


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Surgery_Schwartz. to include neurologic or cardiac disease) is likely deleterious and does not appear to be beneficial. Plac-ing cooling blankets on or under the patient or ice packs in the axillae or groin may be effective in cooling the skin, and when this occurs, a subsequent feedback loop triggers the hypothalamus to raise the internally regulated set point, thus raising core temperature even higher. This paradoxical reac-tion may be why those who feel the need to treat a fever in the ICU by cooling the skin and arguably the core have worse outcomes. Cooling core temperatures can be achieved reli-ably with catheter-directed therapy with commercially avail-able devices. Whether this is a worthwhile practice or not may be controversial. Poor data exist in support of treating fevers lower than 42°C in any fashion.147-149Adult trauma patients who underwent induced hypother-mia had poor outcomes in a recent investigation, and thus, this remains a procedure to be avoided. In a similar vein, pediatric


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Surgery_Schwartz. any fashion.147-149Adult trauma patients who underwent induced hypother-mia had poor outcomes in a recent investigation, and thus, this remains a procedure to be avoided. In a similar vein, pediatric patients who were induced did not show any improvement, and therefore, induced hypothermia is not recommended. Compli-cations with induced hypothermia include, but are not limited to, hypokalemia, diuresis, DVT (due to catheter-related vein injury), arrhythmias, shivering, undiagnosed catheter-related bloodstream infection, and bacteremia.150-152Neurologic dysfunction is inconsistent in hypothermia, but a deterioration in reasoning and decision-making skills progresses as body temperature falls, and profound coma (and a flat electroencephalogram) occurs as the temperature drops below 30°C (86°F). The diagnosis of hypothermia is important, so accurate measurement techniques are required to get a true core temperature.Methods used to warm patients include warm air circu-lation over the


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Surgery_Schwartz. (86°F). The diagnosis of hypothermia is important, so accurate measurement techniques are required to get a true core temperature.Methods used to warm patients include warm air circu-lation over the patient and heated IV fluids, as well as more aggressive measures such as bilateral chest tubes with warm solution lavage, intraperitoneal rewarming lavage, and extra-corporeal membrane oxygenation. A rate of temperature rise of 2°C to 4°C (3.6°F–7.2°F) per hour is considered adequate, but the most common complication for nonbypass rewarming is arrhythmia with ventricular arrest.Hyperthermia. Hyperthermia is defined as a core temperature greater than 38.6°C (101.5°F) and has a host of etiologies (Table 12-19).147 Hyperthermia can be environmentally induced (e.g., summer heat with inability to dissipate heat or control exposure), iatrogenically induced (e.g., heat lamps and medica-tions), endocrine in origin (e.g., thyrotoxicosis), or neurologi-cally induced (i.e., hypothalamic


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Surgery_Schwartz. to dissipate heat or control exposure), iatrogenically induced (e.g., heat lamps and medica-tions), endocrine in origin (e.g., thyrotoxicosis), or neurologi-cally induced (i.e., hypothalamic dysfunction).Malignant hyperthermia occurs intraoperatively after exposure to agents such as succinylcholine and some halothane-based inhalational anesthetics. The presentation is dramatic, with rapid onset of increased temperature, rigors, and myoglo-binuria related to myonecrosis. Medications must be discontin-ued immediately and dantrolene administered (2.5 mg/kg every 5 minutes) until symptoms subside. Aggressive cooling meth-ods are also implemented, such as an alcohol bath, or packing in ice. In cases of severe malignant hyperthermia, the mortality rate is nearly 30%.153,154Thyrotoxicosis can occur after surgery due to undiagnosed Graves’ disease. Hallmarks of the syndrome include hyperther-mia (>40°C [104°F]), anxiety, copious diaphoresis, congestive heart failure (present in about one


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Surgery_Schwartz. occur after surgery due to undiagnosed Graves’ disease. Hallmarks of the syndrome include hyperther-mia (>40°C [104°F]), anxiety, copious diaphoresis, congestive heart failure (present in about one fourth of episodes), tachycar-dia (most commonly atrial fibrillation), and hypokalemia (in up to 50% of patients). The treatment of thyrotoxicosis includes glucocorticoids, propylthiouracil, β-blockade, and iodide (Lugol’s solution) delivered in an emergent fashion. As the name suggests, these patients are usually toxic and require sup-portive measures as well. Acetaminophen, the cooling modali-ties noted in the previous paragraph, and vasoactive agents often are indicated.REFERENCESEntries highlighted in bright blue are key references. 1. Makary MA, Daniel M. Medical error—the third lead-ing cause of death in the US. Brit Med J. 2016;353:i2139. doi:10.1136/bmj.i2139 2. Kohn KT, Corrigan JM, Donaldson MS. To Err Is Human: Building a Safer Health System. Washington, DC: National Academy


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Surgery_Schwartz. cause of death in the US. Brit Med J. 2016;353:i2139. doi:10.1136/bmj.i2139 2. Kohn KT, Corrigan JM, Donaldson MS. To Err Is Human: Building a Safer Health System. Washington, DC: National Academy Press; 1999. 3. James JTA. A new, evidence-based estimate of patient harms associated with hospital care. J Patient Saf. 2013;9:122-128. 4. Lyu H, Xu T, Brotman D, et al. Overtreatment in the U.S. PLOS One. 2017;12(9):e0181970. 5. Makary MA, Overton HN, Wang P. Overprescribing is major contributor to opioid crisis. Brit Med J. 2017;359:j4792. doi: 10.1136/bmj.j4792Table 12-19Common causes of elevated temperature in surgical patientsHYPERTHERMIAHYPERPYREXIAEnvironmentalSepsisMalignant hyperthermiaInfectionNeuroleptic malignant syndromeDrug reactionThyrotoxicosisTransfusion reactionPheochromocytomaCollagen disordersCarcinoid syndromeFactitious syndromeIatrogenicNeoplastic disordersCentral/hypothalamic responses Pulmonary embolism Adrenal insufficiency Brunicardi_Ch12_p0397-p0432.indd


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Surgery_Schwartz. disordersCarcinoid syndromeFactitious syndromeIatrogenicNeoplastic disordersCentral/hypothalamic responses Pulmonary embolism Adrenal insufficiency Brunicardi_Ch12_p0397-p0432.indd 42820/02/19 3:57 PM 429QUALITY, PATIENT SAFETY, ASSESSMENTS OF CARE, AND COMPLICATIONSCHAPTER 12 6. Bierly PE III, Spender JC. Culture and high reliability orga-nizations: the case of the nuclear submarine. J Manage. 1995;21:639-656. 7. Ruchlin HS, Dubbs NL, Callahan MA. The role of leadership in instilling a culture of safety: lessons from the literature. J Healthcare Mgmt. 2004;49:47-58. 8. Perrow C. Normal Accidents: Living with High Risk Technolo-gies. Princeton, NJ: Princeton University Press; 1984. 9. Makary MA, Sexton JB, Freischlag JA, et al. Patient safety in surgery. Ann Surg. 2006;243:628-635. 10. Berenholtz SM, Pronovost PJ. Monitoring patient safety. Crit Care Clin 2007;23:659-673. 11. Baker DP, Gustafson S, Beaubien J, et al. Medical team train-ing. In: Medical Teamwork and Patient


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Surgery_Schwartz. SM, Pronovost PJ. Monitoring patient safety. Crit Care Clin 2007;23:659-673. 11. Baker DP, Gustafson S, Beaubien J, et al. Medical team train-ing. In: Medical Teamwork and Patient Safety: The Evidence-Based Relation. Literature Review. AHRQ Publication No. 05-0053. Rockville, MD: Agency for Healthcare Research and Quality; April 2005. Available at: http://www.ahrq.gov/qual/medteam/medteam4.htm. Accessed November 13, 2012. 12. Pizzi LT, Goldfarb NI, Nash DB. Promoting a culture of safety. In: Making Healthcare Safer: A Critical Analysis of Patient Safety Practices. Evidence Report/Technology Assessment: Number 43. AHRQ Publication No. 01-E058. Rockville, MD: Agency for Healthcare Research and Quality; July 2001. Available at: http://www.ahrq.gov/clinic/ptsafety/chap40.htm. Accessed November 12, 2012. 13. Chan DK, Gallagher TH, Reznick R, Levinson W. How sur-geons disclose medical errors to patients: a study using stan-dardized patients. Surgery. 2005;138:851-858. 14. Sexton JB, Thomas


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Surgery_Schwartz. 12, 2012. 13. Chan DK, Gallagher TH, Reznick R, Levinson W. How sur-geons disclose medical errors to patients: a study using stan-dardized patients. Surgery. 2005;138:851-858. 14. Sexton JB, Thomas EJ, Helmreich RL. Error, stress, and team-work in medicine and aviation: cross sectional surveys. BMJ. 2000;320:745-749. 15. Thomas EJ, Sexton JB, Helmreich RL. Discrepant attitudes about teamwork among critical care nurses and physicians. Crit Care Med. 2003;31:956-959. 16. Amalberti R, Auroy Y, Berwick D, Barach P. Five system barriers to achieving ultrasafe healthcare. Ann Intern Med. 2005;142:756-764. 17. The Joint Commission. Sentinel event statistics. Available at: http://www.jointcommission.org/SentinelEvents/Statistics. Accessed November 8, 2012. 18. Lingard L, Espin S, Whyte S, et al. Communication fail-ures in the operating room: an observational classification of recurrent types and effects. Qual Saf Health Care. 2004;13: 330-334. 19. Christian CK, Gustafson ML, Roth EM, et al. A


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Surgery_Schwartz. fail-ures in the operating room: an observational classification of recurrent types and effects. Qual Saf Health Care. 2004;13: 330-334. 19. Christian CK, Gustafson ML, Roth EM, et al. A prospec-tive study of patient safety in the operating room. Surgery. 2006;139:159-173. 20. Makary MA, Sexton JB, Freischlag JA, et al. Operating room teamwork among physicians and nurses: team-work in the eye of the beholder. J Am Coll Surg. 2006;202: 746-752. 21. Pronovost PJ, Berenholtz SM, Goeschel CA, et al. Creating high reliability in health care organizations. Health Serv Res. 2006;41:1599-1617. 22. Makary MA, Mukherjee A, Sexton JB, et al. Operating room briefings and wrong-site surgery. J Am Coll Surg. 2007;204:236-243. 23. Nundy S, Mukherjee A, Sexton JB, et al. Impact of pre-operative briefings on operating room delays. Arch Surg. 2008;143:1068-1072. 24. Makary MA, Epstein J, Pronovost PJ, Millman EA, Hart-mann EC, Freischlag JA. Surgical specimen identification errors: a new measure of


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Surgery_Schwartz. on operating room delays. Arch Surg. 2008;143:1068-1072. 24. Makary MA, Epstein J, Pronovost PJ, Millman EA, Hart-mann EC, Freischlag JA. Surgical specimen identification errors: a new measure of quality in surgical care. Surgery. 2007;141:450-455. 25. Arora V, Johnson J, Lovinger D, Humphrey H, Meltzer D. Communication failures in patient sign-out and suggestions for improvement: a critical incident analysis. Qual Saf Health Care. 2005;14:401-407. 26. Cooper M, Makary M. A comprehensive unit-based safety program (CUSP) in surgery: improving quality through trans-parency. Surg Clin North Am. 2012;92(1):51-63. 27. Wick ED, Hobson DB, Bennett JL, et al. Implementation of a surgical comprehensive unit-based safety program to reduce surgical site infections. J Am Coll Surg. 2012;215(2):193-200. 28. Makary M, Mehta A, Xu T. Improving wisely using physician metrics. Am J Med Qual. 2018;33(1):103-105. 29. Agency for Healthcare Research and Quality. AHRQ Profile: Quality Research for Quality


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Surgery_Schwartz. DW. The Surgical Infection Prevention and Surgical Care Improvement Projects: promises and pitfalls. Am Surg. 2006;72:1010-1016. 33. The Joint Commission. SCIP Target Areas. Available at: http://www.jointcommission.org/surgical_care_improvement_proj-ect/. Accessed November 1, 2012. 34. Khuri SF. Safety, quality, and the National Surgical Quality Improvement Program. Am Surg. 2006;72:994-998. 35. Hall BL, Hamilton BH, Richards K, Bilimoria KY, Cohen ME, Ko CY. Does surgical quality improve in the American College of Surgeons National Surgical Quality Improvement Program: an evaluation of all participating hospitals. Ann Surg. 2009;250(3):363-376. 36. Brooke BS, Perler BA, Dominici F, Makary MA, Prono-vost PJ. California hospitals meeting Leapfrog quality stan-dards for abdominal aortic aneurysm repair. J Vasc Surg. 2008;47:1155-1164. 37. The Leapfrog Group. Available at:


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Surgery_Schwartz. F, Makary MA, Prono-vost PJ. California hospitals meeting Leapfrog quality stan-dards for abdominal aortic aneurysm repair. J Vasc Surg. 2008;47:1155-1164. 37. The Leapfrog Group. Available at: http://www.leapfrog-group.org/56440/leapfrog_hospital_survey_copy/leapfrog_safety_practices/evidence-based_hospital_referral. Accessed November 7, 2010. 38. World Health Organization. Guidelines for Safe Surgery. Geneva, Switzerland: World Health Organization; 2009. 39. Gawande AA, Kwaan MR, Regenbogen SE, Lipsitz SA, Zinner MJ. An Apgar score for surgery. J Am Coll Surg. 2007;204:201-208. 40. The National Quality Forum. Serious Reportable Events in Healthcare 2011 Update: A Consensus Report. Washington, DC: National Quality Forum; 2011. 41. Mehtsun W, Ibrahim A, Pronovost P, et al. Surgical never events: cost and outcome for patients and providers. Surgery. 2013;153(4):465-472. 42. Crane M. Wrong-site surgery occurs 40 times a week. Med-scape Medical News; 2011. Available at:


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Surgery_Schwartz. Surgical never events: cost and outcome for patients and providers. Surgery. 2013;153(4):465-472. 42. Crane M. Wrong-site surgery occurs 40 times a week. Med-scape Medical News; 2011. Available at: http://www.med-scape.com/viewarticle/745581. Accessed May 12, 2018. 43. Gibbs VC, Coakley FD, Reines HD. Preventable errors in the operating room: retained foreign bodies after surgery—Part 1. Curr Probl Surg. 2007;44(5):281-337. 44. Gawande AA, Studdert DM, Orav EJ, Brennan TA, Zinner MJ. Risk factors for retained instruments and sponges after surgery. N Engl J Med. 2003;34:229-235. 45. Lincourt AE, Harrell A, Cristiano J, Sechrist C, Kercher K, Heniford BT. Retained foreign bodies after surgery. J Surg Res. 2007;138:170-174. 46. Pennsylvania Patient Safety Reporting System. Doing the “right” things to correct wrong-site surgery. Patient Safety Advisory. 2007;4(2):29-45.Brunicardi_Ch12_p0397-p0432.indd 42920/02/19 3:57 PM 430BASIC CONSIDERATIONSPART I 47. Clarke JR, Johnston J, Finley


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Surgery_Schwartz. things to correct wrong-site surgery. Patient Safety Advisory. 2007;4(2):29-45.Brunicardi_Ch12_p0397-p0432.indd 42920/02/19 3:57 PM 430BASIC CONSIDERATIONSPART I 47. Clarke JR, Johnston J, Finley ED. Getting surgery right. Ann Surg. 2007;246:395-405. 48. Kwaan MR, Studdert DM, Zinner MJ, Gawande AA. Inci-dence, patterns, and prevention of wrong-site surgery. Arch Surg. 2006;141:353. 49. Michaels RK, Makary MA, Dahab Y, et al. Achieving the National Quality Forum’s “never events”: prevention of wrong site, wrong procedure, and wrong patient opera-tions. Ann Surg. 2007;245:526-532. 50. Chassin MR. Achieving and sustaining improved quality: lessons from New York state and cardiac surgery. Health Aff. 2002;21(4):40-51. 51. Giordano LA, Elliott MN, Goldstein E, Lehrman WG, Spencer PA. Development, implementation and public reporting of the HCAHPS survey. Med Care Res Rev. 2010;67(1):27-37. 52. Elliott MN, Beckett MK, Lehrman PD, et al. Understanding the role played by Medicare’s


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Surgery_Schwartz. Development, implementation and public reporting of the HCAHPS survey. Med Care Res Rev. 2010;67(1):27-37. 52. Elliott MN, Beckett MK, Lehrman PD, et al. Understanding the role played by Medicare’s patient experience points system in hospital reimbursement. Health Aff. 2016;35(9):1673-1680. 53. Regenbogen SE, Greenberg CC, Studdert DM, Lipsitz SR, Zinner MJ, Gawande AA. Patterns of technical error among surgical malpractice claims: an analysis of strategies to prevent injury to surgical patients. Ann Surg. 2007;246(5):705-711. 54. Griffin FD, Stephens LS, Alexander JB, et al. The American College of Surgeons’ closed claims study: new insights for improving care. J Am Coll Surg. 2007;204(4):561-569. 55. Ambady N, LaPlante D, Nguyen T, Rosenthal R, Chaumeton N, Levinson W. Surgeons’ tone of voice: a clue to malpractice history. Surgery. 2002;132(1):5-9. 56. Woreta TA, Makary MA. Patient safety. In: Makary M, ed. General Surgery Review. Washington, DC: Ladner-Drysdale;


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Surgery_Schwartz. Surgeons’ tone of voice: a clue to malpractice history. Surgery. 2002;132(1):5-9. 56. Woreta TA, Makary MA. Patient safety. In: Makary M, ed. General Surgery Review. Washington, DC: Ladner-Drysdale; 2008:553. 57. Wojcieszak D, Banja J, Houk C. The sorry works! Coalition: making the case for full disclosure. Jt Comm J Qual Patient Saf. 2006;32:344-350. 58. Alemzadeh H, Raman J, Leveson N, Kalbarczyk Z, and Iyer RK. Adverse events in robotic surgery: a retrospective study of 14 years of FDA data. PLoS One. 2016;11(4):e0151470. doi: 10.1371/journal.pone.0151470. 59. Cooper MA, Ibrahim A, Lyu H, Makary MA. Underreport-ing of robotic surgery complications. J Healthcare Qual. 2015;37:133-138. 60. Veenstra DL, Saint S, Sullivan SD. Cost-effectiveness of antiseptic-impregnated central venous catheters for the pre-vention of catheter-related bloodstream infection. JAMA. 1999;282:554-560. 61. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular


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Surgery_Schwartz. catheters for the pre-vention of catheter-related bloodstream infection. JAMA. 1999;282:554-560. 61. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections. Am J Infect Control. 2002;30(8):476-489. 62. Stoiser B, Kofler J, Staudinger T, et al. Contamination of central venous catheters in immunocompromised patients: a comparison between two different types of central venous catheters. J Hosp Infect. 2002;50(3):202-206. 63. Berenholtz S, Pronovost P, Lipsett P, et al. Eliminating cath-eter-related bloodstream infections in the intensive care unit. Crit Care Med. 2004;32(10):2014-2020. 64. Tyroch AH, Kaups K, Lorenzo M, Schreiber M, Solis D. Rou-tine chest radiograph is not indicated after open tracheostomy: a multicenter perspective. Am Surg. 2002;68(1):80-82. 65. Datta D, Onyirimba F, McNamee MJ. The utility of chest radiographs following percutaneous dilatational tracheostomy. Chest. 2003;123:1603-1606. 66. Gelman JJ,


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Surgery_Schwartz. Am Surg. 2002;68(1):80-82. 65. Datta D, Onyirimba F, McNamee MJ. The utility of chest radiographs following percutaneous dilatational tracheostomy. Chest. 2003;123:1603-1606. 66. Gelman JJ, Aro M, Weiss SM. Tracheo-innominate artery fis-tula. J Am Coll Surg. 1994;179:626-634. 67. Keçeligil HT, Erk MK, Kolbakir F, Yildirim A, Yilman M, Ünal R. Tracheoinnominate artery fistula following tracheos-tomy. Cardiovasc Surg. 1995;3:509. 68. Rybak MJ, Abate BJ, Kang SL, Ruffing MJ, Lerner SA, Drusano GL. Prospective evaluation of the effect of an aminoglycoside doing regimen on rates of observed neph-rotoxicity and ototoxicity. Animicrob Agents Chemother. 1999;43(7):1549-1555. 69. Sandur S, Stoller JK. Pulmonary complications of mechanical ventilation. Clin Chest Med. 1999;20:223-247. 70. Hughes MG, Evans HL, Chong TW, et al. Effect of an inten-sive care unit rotating empiric antibiotic schedule on the devel-opment of hospital-acquired infections on the non-intensive care unit ward. Crit Care


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Surgery_Schwartz. Evans HL, Chong TW, et al. Effect of an inten-sive care unit rotating empiric antibiotic schedule on the devel-opment of hospital-acquired infections on the non-intensive care unit ward. Crit Care Med. 2004;32(1):53-60. 71. Horn SD, Wright HL, Couperus JJ, et al. Association between patient-controlled analgesia pump use and postoperative sur-gical site infection in intestinal surgery patients. Surg Infect (Larchmt). 2002;3(2):109-118. 72. Ferguson ND, Fan E, Camporota L, et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplemen-tary material. Intensive Care Med. 2012;38(10):1573-1582. 73. Villar J, Kacmarek RM. The American-European Consensus Conference definition of the acute respiratory distress syn-drome is dead, long live positive end-expiratory pressure! Med Intensiva. 2012;36(8):571-575. 74. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Defini-tion. JAMA.


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Surgery_Schwartz. end-expiratory pressure! Med Intensiva. 2012;36(8):571-575. 74. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Defini-tion. JAMA. 2012;307(23):2526-2533. 75. Thille AW, Esteban A, Fernández-Segoviano P, et al. Com-parison of the Berlin definition for acute respiratory dis-tress syndrome with autopsy. Am J Respir Crit Care Med. 2013;187(7):761-767. 76. The Acute Respiratory Distress Syndrome Network. Ventila-tion with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301-1308. 77. Valente Barbas CS. Lung recruitment maneuvers in acute respiratory distress syndrome and facilitating resolution. Crit Care Med. 2003;31:S265-S271. 78. Singh JM, Stewart TE. High-frequency mechanical ventilation principles and practices in the era of lung-protective ventila-tion strategies. Respir Care Clin North Am. 2002;8:247-260. 79. Yang KL,


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Surgery_Schwartz. JM, Stewart TE. High-frequency mechanical ventilation principles and practices in the era of lung-protective ventila-tion strategies. Respir Care Clin North Am. 2002;8:247-260. 79. Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med. 1991;324:1445-1450. 80. Epstein SK. Etiology of extubation failure and the predictive value of the rapid shallow breathing index. Am J Respir Crit Care Med. 1995;152:545-549. 81. Spaniolas K, Velmahos GC, Wicky S, et al. Is upper extremity deep venous thrombosis underdiagnosed in trauma patients? Am Surg. 2008;74(2):124-128. 82. Dabbagh O, Nagam N, Chitima-Matsiga R, Bearelly S, Bearelly D. Retrievable inferior vena cava filters are not getting retrieved: where is the gap? Thromb Res. 2010;126(6):493-497. 83. Falk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067-1078. 84. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in


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Surgery_Schwartz. Thromb Res. 2010;126(6):493-497. 83. Falk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067-1078. 84. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persis-tent atrial fibrillation. N Engl J Med. 2002;347(23):1834-1840. 85. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347(23):1825-1833. 86. Franklin RH. Ivor Lewis Lecture, 1975. The advancing frontiers of oesophageal surgery. Ann R Coll Surg Engl. 1977;59(4):284-287. 87. Stewart BT, Woods RJ, Collopy BT, Fink RJ, Mackay JR, Keck JO. Early feeding after elective open colorectal resections: a prospective randomized trial. Aust N Z J Surg. 1998;68(2):125-128. 88. Asao T, Kuwano H, Nakamura J, Morinaga N, Hirayama I, Ide M. Gum chewing enhances early recovery from post-operative ileus after laparoscopic colectomy. J Am Coll Surg.


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Surgery_Schwartz. Surg. 1998;68(2):125-128. 88. Asao T, Kuwano H, Nakamura J, Morinaga N, Hirayama I, Ide M. Gum chewing enhances early recovery from post-operative ileus after laparoscopic colectomy. J Am Coll Surg. 2002;195(1):30-32.Brunicardi_Ch12_p0397-p0432.indd 43020/02/19 3:57 PM 431QUALITY, PATIENT SAFETY, ASSESSMENTS OF CARE, AND COMPLICATIONSCHAPTER 12 89. Kelley SR, Wolff BG, Lovely JK, Larson DW. Fast-track path-way for minimally invasive colorectal surgery with and with-out alvimopan (Entereg)(TM): which is more cost-effective? Am Surg. 2013;79(6):630-633. 90. Wang S, Shah N, Philip J, Caraccio T, Feuerman M, Malone B. Role of alvimopan (entereg) in gastrointestinal recov-ery and hospital length of stay after bowel resection. P T. 2012;37(9):518-525. 91. Elsner JL, Smith JM, Ensor CR. Intravenous neostigmine for postoperative acute colonic pseudo-obstruction. Ann Pharma-cother. 2012;46(3):430-435. 92. Tang CL, Seow-Choen F, Fook-Chong S, Eu KW. Bioresorb-able adhesion barrier


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Surgery_Schwartz. CR. Intravenous neostigmine for postoperative acute colonic pseudo-obstruction. Ann Pharma-cother. 2012;46(3):430-435. 92. Tang CL, Seow-Choen F, Fook-Chong S, Eu KW. Bioresorb-able adhesion barrier facilitates early closure of the defunction-ing ileostomy after rectal excision: a prospective, randomized trial. Dis Colon Rectum. 2003;46(9):1200-1207. 93. Beck DE, Cohen Z, Fleshman JW, Kaufman HS, van Goor H, Wolff BG; Adhesion Study Group Steering Committee. A prospective, randomized, multicenter, controlled study of the safety of Seprafilm adhesion barrier in abdominopelvic surgery of the intestine. Dis Colon Rectum. 2003;46(10):1310-1319. 94. Smoot RL, Gostout CJ, Rajan E, et al. Is early colonoscopy after admission for acute diverticular bleeding needed? Am J Gastroenterol. 2003;98:1996-1999. 95. Sorbi D, Gostout CJ, Peura D, et al. An assessment of the management of acute bleeding varices: a multicenter prospective member-based study. Am J Gastroenterol.


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Surgery_Schwartz. Gastroenterol. 2003;98:1996-1999. 95. Sorbi D, Gostout CJ, Peura D, et al. An assessment of the management of acute bleeding varices: a multicenter prospective member-based study. Am J Gastroenterol. 2003;98(11):2424-2434. 96. Domschke W, Lederer P, Lux G. The value of emergency endoscopy in upper gastrointestinal bleeding: review and analysis of 2014 cases. Endoscopy. 1983;15(suppl 1):126-131. 97. Cash BD. Evidence-based medicine as it applies to acid suppression in the hospitalized patient. Crit Care Med. 2002;30(suppl 6):S373-S380. 98. Lidwig K, Bernhardt J, Steffen H, Lorenz D. Contribution of intraoperative cholangiography to incidence and outcome of common bile duct injuries during laparoscopic cholecystec-tomy. Surg Endosc. 2002;16(7):1098-1104. 99. Flum DR, Dellinger EP, Cheadle A, Chan L, Koepsell T. Intra-operative cholangiography and risk of common bile duct injury during cholecystectomy. JAMA. 2003;289(13):1639-1644. 100. Yoon YH, Hsiao-ye Y, Grant BF, Doufour M.


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Surgery_Schwartz. Cheadle A, Chan L, Koepsell T. Intra-operative cholangiography and risk of common bile duct injury during cholecystectomy. JAMA. 2003;289(13):1639-1644. 100. Yoon YH, Hsiao-ye Y, Grant BF, Doufour M. Surveillance Report No. 57: Liver Cirrhosis Mortality in the United States, 1970-98. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism; December 2001. 101. Elmunzer BJ, Scheiman JM, Lehman GA, et al. A randomized trial of rectal indomethacin to prevent post-ERCP pancreatitis. N Engl J Med. 2012;366(15):1414-1422. 102. Solomon R, Werner C, Mann D, D’Elia J, Silva P. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994;331(21):1416-1420. 103. Stevens MA, McCullough PA, Tobin KJ, et al. A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. study. Prevention of Radiocontrast Induced Nephropathy Clinical


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Surgery_Schwartz. A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. study. Prevention of Radiocontrast Induced Nephropathy Clinical Evaluation. J Am Coll Cardiol. 1999;33(2):403-411. 104. Birck R, Krzossok S, Markowetz F, Schnülle P, van der Woude FJ, Braun C. Acetylcysteine for prevention of contrast nephropathy: meta-analysis. Lancet. 2003;362(9384):598-603. 105. Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol. 2003;41(12):2114-2118. 106. Laffan M, O’Connell NM, Perry DJ, et al. Analysis and results of the recombinant factor VIIa extended-use registry. Blood Coagul Fibrinolysis. 2003;14:S35-238. 107. Hedner U. Dosing with recombinant factor VIIa based on cur-rent evidence. Semin Hematol. 2004;41(suppl 1):35-39. 108. Midathada MV, Mehta P, Waner M, Fink LM. Recombinant factor VIIa in the treatment


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Surgery_Schwartz. U. Dosing with recombinant factor VIIa based on cur-rent evidence. Semin Hematol. 2004;41(suppl 1):35-39. 108. Midathada MV, Mehta P, Waner M, Fink LM. Recombinant factor VIIa in the treatment of bleeding. Am J Clin Pathol. 2004;121(1):124-137. 109. Dutton RP, Parr M, Tortella BJ, et al. Recombinant activated factor VII safety in trauma patients: results from the CONTROL trial. J Trauma. 2011;71(1):12-19. 110. Bloomfield GL, Dalton JM, Sugerman HJ, et al. Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma. J Trauma. 1995;39(6):1168-1170. 111. Kron I, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg. 1984;199(1):28-30. 112. Ivatury RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and


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Surgery_Schwartz. RR, Porter JM, Simon RJ, et al. Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma. 1998;44(6):1016-1021. 113. Ivatury RR, Sugerman HJ, Peitzman AB. Abdominal com-partment syndrome: recognition and management. Adv Surg. 2001;35:251-269. 114. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdom-inal compartment syndrome. J Trauma. 1998;45(3):597-609. 115. Anglen J, Apostoles PS, Christensen G, Gainor B, Lane J. Removal of surface bacteria by irrigation. J Orthop Res. 1966;14:251-254. 116. Lewis DA, Leaper DJ, Speller DC. Prevention of bacterial colonization of wounds at operation: comparison of iodine-impregnated (“Ioban”) drapes with conventional methods. J Hosp Infect. 1984;5:431-437. 117. O’Rourke E, Runyan D, O’Leary J, Stern J. Contami-nated iodophor in the operating room. Am J Infect Control. 2003;31:255-256. 118. Ostrander RV,


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Surgery_Schwartz. methods. J Hosp Infect. 1984;5:431-437. 117. O’Rourke E, Runyan D, O’Leary J, Stern J. Contami-nated iodophor in the operating room. Am J Infect Control. 2003;31:255-256. 118. Ostrander RV, Brage ME, Botte MJ. Bacterial skin contamina-tion after surgical preparation in foot and ankle surgery. Clin Orthop. 2003;406:246-252. 119. Ghogawala Z, Furtado D. In vitro and in vivo bactericidal activities of 10%, 2.5%, and 1% povidone-iodine solution. Am J Hosp Pharm. 1990;47:1562-1566. 120. Anderson RL, Vess RW, Carr JH, Bond WW, Panlilio AL, Favero MS. Investigations of intrinsic Pseudomonas cepa-cia contamination in commercially manufactured povidone-iodine. Infect Control Hosp Epidemiol. 1991;12(5):297-302. 121. Birnbach DJ, Meadows W, Stein DJ, Murray O, Thys DM, Sor-dillo EM. Comparison of povidone iodine and DuraPrep, an iodophor-in-isopropyl alcohol solution, for skin disinfection prior to epidural catheter insertion in parturients. Anesthesiol-ogy. 2003;98(1):164-169. 122. Moen MD,


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Surgery_Schwartz. povidone iodine and DuraPrep, an iodophor-in-isopropyl alcohol solution, for skin disinfection prior to epidural catheter insertion in parturients. Anesthesiol-ogy. 2003;98(1):164-169. 122. Moen MD, Noone MG, Kirson I. Povidone-iodine spray technique versus traditional scrub-paint technique for pre-operative abdominal wall preparation. Am J Obstet Gynecol. 2002;187(6):1434-1436; discussion 1436-1437. 123. Strand CL, Wajsbort RR, Sturmann K. Effect of iodophor vs iodine tincture skin preparation on blood culture contamina-tion rate. JAMA. 1993;269(8):1004-1006. 124. Paterson DL, Ko WC, Von Gottberg A, et al. International pro-spective study of Klebsiella pneumoniae bacteremia: impli-cations of extended-spectrum beta-lactamase production in nosocomial infections. Ann Intern Med. 2004;140(1):26-32. 125. Wittmann DH, Schein M. Let us shorten antibiotic prophylaxis and therapy in surgery. Am J Surg. 1966;172(6A):26S-32S. 126. Dellinger EP. Duration of antibiotic treatment in surgical


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Surgery_Schwartz. DH, Schein M. Let us shorten antibiotic prophylaxis and therapy in surgery. Am J Surg. 1966;172(6A):26S-32S. 126. Dellinger EP. Duration of antibiotic treatment in surgical infec-tions of the abdomen. Undesired effects of antibiotics and future studies. Eur J Surg Suppl. 1996;576:29-31; discussion 31. 127. Fry DE. Basic aspects of and general problems in surgical infections. Surg Infect (Larchmt). 2001;2(suppl 1):S3-S11. 128. Barie PS. Modern surgical antibiotic prophylaxis and therapy—less is more. Surg Infect (Larchmt). 2000;1:23-29.Brunicardi_Ch12_p0397-p0432.indd 43120/02/19 3:57 PM 432BASIC CONSIDERATIONSPART I 129. Grobmyer SR, Graham D, Brennan MF, Coit D. High-pressure gradients generated by closed-suction surgical drainage sys-tems. Surg Infect (Larchmt). 2002;3(3):245-249. 130. Power DA, Duggan J, Brady HR. Renal-dose (low-dose) dopa-mine for the treatment of sepsis-related and other forms of acute renal failure: ineffective and probably dangerous. Clin Exp Pharmacol


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Surgery_Schwartz. DA, Duggan J, Brady HR. Renal-dose (low-dose) dopa-mine for the treatment of sepsis-related and other forms of acute renal failure: ineffective and probably dangerous. Clin Exp Pharmacol Physiol Suppl. 1999;26:S23-S28. 131. Vincent JL, Abraham E, Annane D, Bernard G, Rivers E, Van de Berghe G. Reducing mortality in sepsis: new directions. Crit Care. 2002;6(suppl 3):S1-S18. 132. Malay MB, Ashton RC Jr, Landry DW, Townsend RN. Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma. 1999;47:699-703; discussion 703-705. 133. Annane D, Sebille V, Charpentier C, et al. Effect of treat-ment with low doses of hydrocortisone and fludrocorti-sone on mortality in patients with septic shock. JAMA. 2002;288(7):862-871. 134. Dhainaut JF, Laterre PF, LaRosa SP, et al. The clinical evaluation committee in a large multicenter phase 3 trial of drotrecogin alfa (activated) in patients with severe sepsis (PROWESS): role, methodology, and results. Crit Care Med. 2003;31(9):2291-2301;


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Surgery_Schwartz. committee in a large multicenter phase 3 trial of drotrecogin alfa (activated) in patients with severe sepsis (PROWESS): role, methodology, and results. Crit Care Med. 2003;31(9):2291-2301; comment 2405. 135. Betancourt M, McKinnon PS, Massanari RM, Kanji S, Bach D, Devlin JW. An evaluation of the cost effectiveness of drotrecogin alfa (activated) relative to the number of organ system failures. Pharmacoeconomics. 2003;21:1331-1340. 136. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;345(19):1359-1367. 137. Finney SJ, Zekveld C, Elia A, Evans TW. Glucose con-trol and mortality in critically ill patients. JAMA. 2003;290(15):2041-2047. 138. Furnary AP, Gao G, Grunkemeier GL, et al. Continuous insu-lin infusion reduces mortality in patients with diabetes under-going coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2003;125(5):1007-1021. 139. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, et al.


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Surgery_Schwartz. mortality in patients with diabetes under-going coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2003;125(5):1007-1021. 139. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283-1297. 140. COIITSS Study Investigators, Annane D, Cariou A, et al. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomized controlled trial. JAMA. 2010;303(4):341-348. 141. Saberi F, Heyland D, Lam M, et al. Prevalence, incidence, and clinical resolution of insulin resistance in critically ill patients: an observational study. JPEN J Parenter Enteral Nutr. 2008;32(3):227-235. 142. Arabi YM, Dabbagh OC, Tamim HM, et al. Intensive versus conventional insulin therapy: a randomized controlled trial in medical and surgical critically ill patients. Crit Care Med. 2008;36(12):3190-3197. 143. La Rochelle GE, Jr, La Rochelle AG, Ratner RE, Borenstein DG.


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Surgery_Schwartz. therapy: a randomized controlled trial in medical and surgical critically ill patients. Crit Care Med. 2008;36(12):3190-3197. 143. La Rochelle GE, Jr, La Rochelle AG, Ratner RE, Borenstein DG. Recovery of the hypothalamic-pituitary-adrenal axis in patients with rheumatic diseases receiving low-dose predni-sone. Am J Med. 1993;95(3):258-264. 144. Bromberg JS, Alfrey EJ, Barker CF, et al. Adrenal suppres-sion and steroid supplementation in renal transplant recipients. Transplantation. 1991;51(2):385-390. 145. Friedman RJ, Schiff CF, Bromberg JS. Use of supplemental steroids in patients having orthopaedic operations. J Bone Joint Surg. 1995;77(12):1801-1806. 146. Kempainen RR, Brunette DD. The evaluation and management of accidental hypothermia. Respir Care. 2004;49(2):192-205. 147. Niven DJ, Stelfox HT, Léger C, et al. Assessment of the safety and feasibility of administering antipyretic therapy in criti-cally ill adults: a pilot randomized clinical trial. J Crit Care.


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Surgery_Schwartz. DJ, Stelfox HT, Léger C, et al. Assessment of the safety and feasibility of administering antipyretic therapy in criti-cally ill adults: a pilot randomized clinical trial. J Crit Care. 2013;28(3):296-302. 148. Schortgen F, Clabault K, Katsahian S, et al. Fever control using external cooling in septic shock: a randomized controlled trial. Am J Respir Criti Care Med. 2012;185(10):1088-1095. 149. Hoedemaekers CW, Ezzahti M, Gerritsen A, van der Hoeven JG. Comparison of cooling methods to induce and main-tain normoand hypothermia in intensive care unit patients: a prospective intervention study. Crit Care (London). 2007;11(4):R91. 150. O’Donnell J, Axelrod P, Fisher C, et al. Use and effectiveness of hypothermia blankets for febrile patients in the intensive care unit. Clin Infect Dis. 1997;24(6):1208-1213. 151. Adelson PD, Wisniewski SR, Beca J, et al. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised con-trolled


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Surgery_Schwartz. PD, Wisniewski SR, Beca J, et al. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised con-trolled trial. Lancet Neurol. 2013;12(6):546-553. 152. Georgiou AP, Manara AR. Role of therapeutic hypothermia in improving outcome after traumatic brain injury: a systematic review. Br J Anaesth. 2013;110(3):357-367. 153. Peterson K, Carson S, Carney N. Hypothermia treatment for traumatic brain injury: a systematic review and meta-analysis. J Neurotrauma. 2008;25(1):62-71. 154. Schulman CI, Namias N, Doherty J, et al. The effect of anti-pyretic therapy upon outcomes in critically ill patients: a ran-domized, prospective study. Surg Infect. 2005;6(4):369-375.Brunicardi_Ch12_p0397-p0432.indd 43220/02/19 3:57 PM


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Surgery_Schwartz. Physiologic Monitoring of the Surgical PatientAnthony R. Cyr and Louis H. Alarcon 13chapterINTRODUCTIONThe Latin verb monere, which means “to warn, or advise” is the origin for the English word monitor. In modern medical prac-tice, patients undergo monitoring to detect pathologic varia-tions in physiologic parameters, providing advanced warning of impending deterioration in the status of one or more organ systems. The intended goal of this endeavor is to allow the clini-cian to take appropriate actions in a timely fashion to prevent or ameliorate the physiologic derangement. Furthermore, physi-ologic monitoring is used not only to warn, but also to titrate therapeutic interventions, such as fluid resuscitation or the infu-sion of vasoactive or inotropic drugs. The intensive care unit (ICU) and operating room are the two locations where the most advanced monitoring capabilities are routinely employed in the care of critically ill patients.In the broadest sense, physiologic monitoring


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Surgery_Schwartz. and operating room are the two locations where the most advanced monitoring capabilities are routinely employed in the care of critically ill patients.In the broadest sense, physiologic monitoring encom-passes a spectrum of endeavors, ranging in complexity from the routine and intermittent measurement of the classic vital signs (i.e., temperature, heart rate, arterial blood pressure, and respira-tory rate) to the continuous recording of the oxidation state of cytochrome oxidase, the terminal element in the mitochondrial electron transport chain. The ability to assess clinically relevant parameters of tissue and organ status and employ this knowl-edge to improve patient outcomes represents the “holy grail” of critical care medicine. Unfortunately, consensus is often lacking regarding the most appropriate parameters to monitor in order to achieve this goal. Furthermore, making an inappropriate ther-apeutic decision due to inaccurate physiologic data or misinter-pretation of good data


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Surgery_Schwartz. most appropriate parameters to monitor in order to achieve this goal. Furthermore, making an inappropriate ther-apeutic decision due to inaccurate physiologic data or misinter-pretation of good data can lead to a worse outcome than having no data at all. Of the highest importance is the integration of physiologic data obtained from monitoring into a coherent and evidenced-based treatment plan. Current technologies available to assist the clinician in this endeavor are summarized in this chapter. Also presented is a brief look at emerging tech-niques that may soon enter into clinical practice.In essence, the goal of hemodynamic monitoring is to ensure that the flow of oxygenated blood through the microcir-culation is sufficient to support aerobic metabolism at the cel-lular level. In general, mammalian cells cannot store oxygen for subsequent use in oxidative metabolism, although a relatively tiny amount is stored in muscle tissue as oxidized myoglobin. Thus, aerobic synthesis of


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Surgery_Schwartz. general, mammalian cells cannot store oxygen for subsequent use in oxidative metabolism, although a relatively tiny amount is stored in muscle tissue as oxidized myoglobin. Thus, aerobic synthesis of adenosine triphosphate (ATP), the energy “currency” of cells, requires the continuous delivery of oxygen by diffusion from hemoglobin in red blood cells to the oxidative machinery within mitochondria. Delivery of oxygen to mitochondria may be insufficient for several reasons. For example, cardiac output, hemoglobin concentration of blood, or the oxygen content of arterial blood each can be inadequate 1Introduction 433Arterial Blood Pressure 434Noninvasive Measurement of Arterial Blood Pressure / 434Invasive Monitoring of Arterial Blood Pressure / 435Electrocardiographic Monitoring 435Algorithmic Integrative Monitoring 436Cardiac Output and Related Parameters 436Determinants of Cardiac Performance / 436Placement of the Pulmonary Artery Catheter 437Hemodynamic


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Surgery_Schwartz. Monitoring 435Algorithmic Integrative Monitoring 436Cardiac Output and Related Parameters 436Determinants of Cardiac Performance / 436Placement of the Pulmonary Artery Catheter 437Hemodynamic Measurements 438Measurement of Cardiac Output by Thermodilution / 439Mixed Venous Oximetry / 439Effect of Pulmonary Artery Catheterization on Outcome 440Minimally Invasive Alternatives to the Pulmonary Artery Catheter 442Transpulmonary Thermodilution / 442Doppler Ultrasonography / 443Impedance Cardiography / 443Pulse Contour Analysis / 443Partial Carbon Dioxide Rebreathing / 444Transesophageal Echocardiography / 444Assessing Preload Responsiveness / 444Near-Infrared Spectroscopic Measurement of Tissue Hemoglobin Oxygen Saturation / 444Respiratory Monitoring 445Arterial Blood Gases / 445Determinants of Oxygen Delivery / 445Peak and Plateau Airway Pressure / 446Pulse Oximetry / 446Pulse CO-Oximetry / 446Capnometry /447Renal Monitoring 447Urine Output / 447Bladder Pressure /


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Surgery_Schwartz. / 445Determinants of Oxygen Delivery / 445Peak and Plateau Airway Pressure / 446Pulse Oximetry / 446Pulse CO-Oximetry / 446Capnometry /447Renal Monitoring 447Urine Output / 447Bladder Pressure / 447Neurologic Monitoring 447Intracranial Pressure / 447Electroencephalogram and Evoked Potentials / 448Transcranial Doppler Ultrasonography / 448Jugular Venous Oximetry / 448Transcranial Near-Infrared Spectroscopy / 449Brain Tissue Oxygen Tension / 449Conclusions 449Brunicardi_Ch13_p0433-p0452.indd 43322/02/19 2:20 PM 434Figure 13-1. Graphical representation of the relationship between oxygen utilization (VO2) and oxygen delivery (DO2). Under most normal physiologic conditions oxygen utilization does not depend on oxygen delivery, but below the critical value DO2crit oxygen utili-zation decreases linearly as a function of oxygen delivery, rendering tissues susceptible to ischemic injury.Key Points1 The delivery of modern critical care is predicated on the abil-ity to monitor a large


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Surgery_Schwartz. decreases linearly as a function of oxygen delivery, rendering tissues susceptible to ischemic injury.Key Points1 The delivery of modern critical care is predicated on the abil-ity to monitor a large number of physiologic variables and formulate evidenced-based therapeutic strategies to manage these variables. Technological advances in monitoring have at least a theoretical risk of exceeding our ability to under-stand the clinical implications of the derived information. This could result in the use of monitoring data to make inap-propriate clinical decisions. Therefore, the implementation of any new monitoring technology must take into account the relevance and accuracy of the data obtained, the risks to the patient, and the evidence supporting any intervention directed at correcting the detected abnormality.2 The routine use of invasive monitoring devices, specifically the pulmonary artery catheter, must be questioned in light of the available evidence that does not demonstrate a


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Surgery_Schwartz. detected abnormality.2 The routine use of invasive monitoring devices, specifically the pulmonary artery catheter, must be questioned in light of the available evidence that does not demonstrate a clear ben-efit to its widespread use in various populations of critically ill patients. The future of physiologic monitoring will be dominated by the application of noninvasive and highly accurate devices which guide evidenced-based therapy.for independent reasons. Alternatively, despite adequate cardiac output, perfusion of capillary networks can be impaired as a consequence of dysregulation of arteriolar tone, microvascular thrombosis, or obstruction of nutritive vessels by sequestered leukocytes or platelets. Hemodynamic monitoring that does not take into account all of these factors will portray an incomplete and perhaps misleading picture of cellular physiology.Under normal conditions when the supply of oxygen is plentiful, aerobic metabolism is determined by factors other than the


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Surgery_Schwartz. portray an incomplete and perhaps misleading picture of cellular physiology.Under normal conditions when the supply of oxygen is plentiful, aerobic metabolism is determined by factors other than the availability of oxygen. These factors include the hor-monal milieu and mechanical workload of contractile tissues. However, in pathologic circumstances when oxygen availabil-ity is inadequate, oxygen utilization (VO2) becomes dependent upon oxygen delivery (DO2). The relationship of VO2 to DO2 over a broad range of DO2 values is commonly represented as two intersecting straight lines (Fig. 13-1). In the region of higher DO2 values, the slope of the line is approximately equal to zero, indicating that VO2 is largely independent of DO2. In contrast, in the region of low DO2 values, the slope of the line is nonzero and positive, indicating that VO2 is supply-dependent. The region where the two lines intersect is called the point of critical oxy-gen delivery (DO2crit), and represents the


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Surgery_Schwartz. of the line is nonzero and positive, indicating that VO2 is supply-dependent. The region where the two lines intersect is called the point of critical oxy-gen delivery (DO2crit), and represents the transition from supplyindependent to supply-dependent oxygen uptake. Below a critical Oxygen delivery, DO2Tissue hypoxiaSupply-dependentoxygen consumptionSupply-independentoxygen consumptionTissue normoxiaOxygen utilization, VO2DO2critthreshold of oxygen delivery, increased oxygen extraction can-not compensate for the delivery deficit; hence, oxygen con-sumption begins to decrease. The slope of the supply-dependent region of the plot reflects the maximal oxygen extraction capa-bility of the vascular bed being evaluated.The subsequent sections will describe the techniques and utility of monitoring various physiologic parameters.ARTERIAL BLOOD PRESSUREThe pressure exerted by blood in the systemic arterial system, commonly referred to simply as “blood pressure,” is a cardinal parameter


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Surgery_Schwartz. various physiologic parameters.ARTERIAL BLOOD PRESSUREThe pressure exerted by blood in the systemic arterial system, commonly referred to simply as “blood pressure,” is a cardinal parameter measured as part of the hemodynamic monitoring of patients. Extremes in blood pressure are either intrinsically deleterious or are indicative of a serious perturbation in normal physiology. Arterial blood pressure is a complex function of both cardiac output and vascular input impedance. Thus, inex-perienced clinicians may assume that the presence of a normal blood pressure is evidence that cardiac output and tissue perfu-sion are adequate. This assumption is frequently incorrect and is the reason why some critically ill patients may benefit from forms of hemodynamic monitoring in addition to measurement of arterial pressure.Blood pressure can be determined directly by measuring the pressure within the arterial lumen or indirectly using a cuff around an extremity. When the equipment is properly set


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Surgery_Schwartz. of arterial pressure.Blood pressure can be determined directly by measuring the pressure within the arterial lumen or indirectly using a cuff around an extremity. When the equipment is properly set up and calibrated, direct intra-arterial monitoring of blood pressure pro-vides accurate and continuous data. Additionally, intra-arterial catheters provide a convenient way to obtain samples of blood for measurements of arterial blood gases and other laboratory studies. Despite these advantages, intra-arterial catheters are invasive devices and occasionally are associated with serious complications.Noninvasive Measurement of Arterial Blood PressureBoth manual and automated means for the noninvasive determi-nation of blood pressure use an inflatable sphygmomanometer cuff to increase pressure around an extremity and to detect the presence or absence of arterial pulsations. Several methods exist for this purpose. The time-honored approach is the auscultation of the Korotkoff sounds, which are


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Surgery_Schwartz. an extremity and to detect the presence or absence of arterial pulsations. Several methods exist for this purpose. The time-honored approach is the auscultation of the Korotkoff sounds, which are heard over an artery distal to the cuff as the cuff is deflated from a pressure higher than systolic pressure to one less than diastolic pressure. Systolic pressure is defined as the pressure in the cuff when tapping sounds are first audible. Diastolic pressure is the pressure in the cuff when audible pulsations first disappear.Brunicardi_Ch13_p0433-p0452.indd 43422/02/19 2:20 PM 435PHYSIOLOGIC MONITORING OF THE SURGICAL PATIENTCHAPTER 13Another means for pulse detection when measuring blood pressure noninvasively depends upon the detection of oscillations in the pressure within the bladder of the cuff. This approach is simple, and unlike auscultation, can be performed even in a noisy environment (e.g., a busy emergency depart-ment or medical helicopter). Unfortunately, this approach is


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Surgery_Schwartz. of the cuff. This approach is simple, and unlike auscultation, can be performed even in a noisy environment (e.g., a busy emergency depart-ment or medical helicopter). Unfortunately, this approach is neither accurate nor reliable. Other methods, however, can be used to reliably detect the reappearance of a pulse distal to the cuff and thereby estimate systolic blood pressure. Two excellent and widely available approaches for pulse detection are use of a Doppler stethoscope (reappearance of the pulse produces an audible amplified signal) or a pulse oximeter (reappearance of the pulse is indicated by flashing of a light-emitting diode).A number of automated devices are capable of repeti-tively measuring blood pressure noninvasively. Some of these devices measure pressure oscillations in the inflatable bladder encircling the extremity to detect arterial pulsations as pressure in the cuff is gradually lowered from greater than systolic to less than diastolic pressure. Other automated


Surgery_Schwartz

Surgery_Schwartz. the inflatable bladder encircling the extremity to detect arterial pulsations as pressure in the cuff is gradually lowered from greater than systolic to less than diastolic pressure. Other automated noninvasive devices use a piezoelectric crystal positioned over the brachial artery as a pulse detector. The accuracy of these devices is variable, and often dependent on the size mismatch between the arm cir-cumference and the cuff size.1 If the cuff is too narrow (relative to the extremity), the measured pressure will be artifactually elevated. Therefore, the width of the cuff should be approxi-mately 40% of its circumference.Another noninvasive approach for measuring blood pres-sure relies on a technique called photoplethysmography. This method is capable of providing continuous information, since systolic and diastolic blood pressures are recorded on a beat-to-beat basis. Photoplethysmography uses the transmission of infrared light to estimate the amount of hemoglobin (directly related


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Surgery_Schwartz. since systolic and diastolic blood pressures are recorded on a beat-to-beat basis. Photoplethysmography uses the transmission of infrared light to estimate the amount of hemoglobin (directly related to the volume of blood) in a finger placed under a servo-controlled inflatable cuff. A feedback loop controlled by a microprocessor continually adjusts the pressure in the cuff to maintain the blood volume of the finger constant. Under these conditions, the pressure in the cuff reflects the pressure in the digi-tal artery. The measurements obtained using photoplethysmog-raphy generally agree closely with those obtained by invasive monitoring of blood pressure.2 However, these readings may be less accurate in patients with hypotension or hypothermia.Invasive Monitoring of Arterial Blood PressureDirect and continuous monitoring of arterial pressure in criti-cally ill patients may be performed by using fluid-filled tubing to connect an intra-arterial catheter to an external strain-gauge


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Surgery_Schwartz. and continuous monitoring of arterial pressure in criti-cally ill patients may be performed by using fluid-filled tubing to connect an intra-arterial catheter to an external strain-gauge transducer. The signal generated by the transducer is electroni-cally amplified and displayed as a continuous waveform by an oscilloscope or computerized display. Digital values for systolic and diastolic pressure also are displayed. Mean pressure, calcu-lated by electronically averaging the amplitude of the pressure waveform, can also be displayed. The fidelity of the catheter-tubing-transducer system is determined by numerous factors, including the compliance of the tubing, the surface area of the transducer diaphragm, and the compliance of the diaphragm. If the system is underdamped, then the inertia of the system, which is a function of the mass of the fluid in the tubing and the mass of the diaphragm, causes overshoot of the points of maximum positive and negative displacement of the diaphragm


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Surgery_Schwartz. of the system, which is a function of the mass of the fluid in the tubing and the mass of the diaphragm, causes overshoot of the points of maximum positive and negative displacement of the diaphragm during sys-tole and diastole, respectively. Thus, in an underdamped system, systolic pressure will be overestimated and diastolic pressure will be underestimated. In an overdamped system, displacement of the diaphragm fails to track the rapidly changing pressure waveform, and systolic pressure will be underestimated and diastolic pressure will be overestimated. It is important to note that even in an underdamped or overdamped system, mean pres-sure will be accurately recorded, provided the system has been properly calibrated. For these reasons, when using direct mea-surement of intra-arterial pressure to monitor patients, clinicians should make clinical decisions based primarily on the measured mean arterial blood pressure.The radial artery at the wrist is the site most commonly used for


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Surgery_Schwartz. pressure to monitor patients, clinicians should make clinical decisions based primarily on the measured mean arterial blood pressure.The radial artery at the wrist is the site most commonly used for intra-arterial pressure monitoring. Other sites include the femoral and axillary artery. It is important to recognize, however, that measured arterial pressure is determined in part by the site where the pressure is monitored. Central (i.e., aortic) and peripheral (e.g., radial artery) pressures typically are dif-ferent as a result of the impedance and inductance of the arte-rial tree. Systolic pressures typically are higher and diastolic pressures are lower in the periphery, whereas mean pressure is approximately the same in the aorta and more distal sites.Distal ischemia is an uncommon complication of intra-arterial catheterization. The incidence of thrombosis is increased when larger-caliber catheters are employed and when catheters are left in place for an extended period of time. The


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Surgery_Schwartz. of intra-arterial catheterization. The incidence of thrombosis is increased when larger-caliber catheters are employed and when catheters are left in place for an extended period of time. The incidence of thrombosis can be minimized by using a 20-gauge (or smaller) catheter in the radial artery and removing the catheter as soon as feasible. The risk of distal ischemic injury can be reduced by ensuring that adequate collateral flow is present prior to catheter insertion. At the wrist, adequate collateral flow can be documented by performing a modified version of the Allen test, wherein the artery to be cannulated is digitally compressed while using a Doppler stethoscope to listen for perfusion in the palmar arch vessels.Another potential complication of intra-arterial monitor-ing is retrograde embolization of air bubbles or thrombi into the intracranial circulation. In order to minimize this risk care should be taken to avoid flushing arterial lines when air is pres-ent in the system,


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Surgery_Schwartz. embolization of air bubbles or thrombi into the intracranial circulation. In order to minimize this risk care should be taken to avoid flushing arterial lines when air is pres-ent in the system, and only small volumes of fluid (less than 5 mL) should be employed for this purpose. Catheter-related infections can occur with any intravascular monitoring device. However, catheter-related bloodstream infection is a relatively uncommon complication of intra-arterial lines used for monitor-ing, occurring in 0.4% to 0.7% of catheterizations.3 The inci-dence increases with longer duration of arterial catheterization.ELECTROCARDIOGRAPHIC MONITORINGThe electrocardiogram (ECG) records the electrical activity associated with cardiac contraction by detecting voltages on the body surface. A standard 3-lead ECG is obtained by placing electrodes that correspond to the left arm (LA), right arm (RA), and left leg (LL). The limb leads are defined as lead I (LA-RA), lead II (LL-RA), and lead III (LL-LA).


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Surgery_Schwartz. ECG is obtained by placing electrodes that correspond to the left arm (LA), right arm (RA), and left leg (LL). The limb leads are defined as lead I (LA-RA), lead II (LL-RA), and lead III (LL-LA). The ECG waveforms can be continuously displayed on a monitor, and the devices can be set to sound an alarm if an abnormality of rate or rhythm is detected. Continuous ECG monitoring is widely available and applied to critically ill and perioperative patients. Monitoring of the ECG waveform is essential in patients with acute coronary syndromes or blunt myocardial injury because dysrhythmias are the most common lethal complication. In patients with shock or sepsis, dysrhythmias can occur as a consequence of inadequate myocardial oxygen delivery or as a complication of vasoactive or inotropic drugs used to support blood pressure and cardiac Brunicardi_Ch13_p0433-p0452.indd 43522/02/19 2:20 PM 436BASIC CONSIDERATIONSPART Ioutput. Dysrhythmias can be detected by continuously moni-toring the


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Surgery_Schwartz. used to support blood pressure and cardiac Brunicardi_Ch13_p0433-p0452.indd 43522/02/19 2:20 PM 436BASIC CONSIDERATIONSPART Ioutput. Dysrhythmias can be detected by continuously moni-toring the ECG tracing, and timely intervention may prevent serious complications. With appropriate computing hardware and software, continuous ST-segment analysis also can be per-formed to detect ischemia or infarction.Additional information can be obtained from a 12-lead ECG, which is essential for patients with potential myocardial ischemia or to rule out cardiac complications in other acutely ill patients. Continuous monitoring of the 12-lead ECG may be beneficial in certain patient populations. In a study of 185 vas-cular surgical patients, continuous 12-lead ECG monitoring was able to detect transient myocardial ischemic episodes in 20.5% of the patients.4 This study demonstrated that the precordial lead V4, which is not routinely monitored on a standard 3-lead ECG, is the most sensitive for


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Surgery_Schwartz. myocardial ischemic episodes in 20.5% of the patients.4 This study demonstrated that the precordial lead V4, which is not routinely monitored on a standard 3-lead ECG, is the most sensitive for detecting perioperative ischemia and infarction. To detect 95% of the ischemic episodes, two or more precordial leads were necessary. Furthermore, in a pro-spective observational study, 51 peripheral artery vascular sur-gery patients underwent ambulatory continuous 12-lead ECG monitoring in the postoperative setting. Ischemic load, defined as the area under the curve defined by ischemic ST-segment deviation and ischemic time, was shown to predict perioperative myocardial infarction with an area under the receiver operating characteristics curve of 0.87. Notably, ischemia was asymptom-atic in 14 of the 17 identified patients, demonstrating value of this modality as a warning tool.5 Thus, continuous 12-lead ECG monitoring may provide greater sensitivity than 3-lead ECG for the detection of


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Surgery_Schwartz. 14 of the 17 identified patients, demonstrating value of this modality as a warning tool.5 Thus, continuous 12-lead ECG monitoring may provide greater sensitivity than 3-lead ECG for the detection of perioperative myocardial ischemia, and may become standard for monitoring high-risk surgical patients.Currently, there is considerable interest in using comput-erized approaches to analyze ECG waveforms and patterns to uncover hidden information that can be used to predict sudden cardiac death or the development of serious dysrhythmias. ECG patterns of interest include repetitive changes in the morphol-ogy of the T-wave (T-wave alternans; TWA)6 and heart rate variability.7ALGORITHMIC INTEGRATIVE MONITORINGIntegrated monitoring systems employ software that integrates vital signs to produce a single-parameter index that allows early detection of physiologic perturbations. The input variables include noninvasive measurements of heart rate, respiratory rate, blood pressure, SpO2, and


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Surgery_Schwartz. a single-parameter index that allows early detection of physiologic perturbations. The input variables include noninvasive measurements of heart rate, respiratory rate, blood pressure, SpO2, and temperature. The software uses neural networking to develop a probabilistic model of normal-ity, previously developed from a representative sample patient training set. Variance from this data set is used to evaluate the probability that the patient-derived vital signs are within the normal range. An abnormal index can occur while no single vital sign parameter is outside the range of normal if their com-bined patterns are consistent with known instability patterns. Employing such an integrated monitoring system in step-down unit patients has been shown to be a sensitive method to detect early physiologic abnormalities that may precede hemodynamic instability.8 This subsequently was demonstrated to reduce the amount of overall patient instability by facilitating earlier iden-tification and


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Surgery_Schwartz. physiologic abnormalities that may precede hemodynamic instability.8 This subsequently was demonstrated to reduce the amount of overall patient instability by facilitating earlier iden-tification and appropriate intervention by the medical team.9The large expansion of the electronic medical record (EMR) is also driving the development of new algorithmic assessment tools for inpatient monitoring. The Rothman Index (RI) is a proprietary data analysis toolkit encompassing a total of 26 variables including vital signs, nursing assessments, laboratory test values, and cardiac rhythms and was developed to make use of the vast amount of data input into the EMR on a real-time basis to help provide a global assessment of patient status. In the initial derivation, Rothman and colleagues dem-onstrated concordance of the RI with the Modified Early Warning Score (MEWS) system, which is designed to alert medical teams to clinical deterioration that precedes cardiac or pulmonary arrest events.10


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Surgery_Schwartz. concordance of the RI with the Modified Early Warning Score (MEWS) system, which is designed to alert medical teams to clinical deterioration that precedes cardiac or pulmonary arrest events.10 Subsequent publications evaluated performance of the RI in predicting both readmission to surgical ICUs in the postoperative setting as well as for rapid response team activations.11-13 Although more work is required to evalu-ate the broad applicability of the RI and similar measures, the evidence to date is compelling. Furthermore, as EMR interfaces become more sophisticated, other real-time data analysis soft-ware packages will likely be developed that provide further insight into the care of postsurgical patients.CARDIAC OUTPUT AND RELATED PARAMETERSBedside catheterization of the pulmonary artery was introduced into clinical practice in the 1970s. Although the pulmonary artery catheter initially was used primarily to manage patients with cardiogenic shock and other acute cardiac diseases,


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Surgery_Schwartz. was introduced into clinical practice in the 1970s. Although the pulmonary artery catheter initially was used primarily to manage patients with cardiogenic shock and other acute cardiac diseases, indi-cations for this form of invasive hemodynamic monitoring gradually expanded to encompass a wide variety of clinical con-ditions. Clearly, many clinicians believe that information valu-able for the management of critically ill patients is afforded by having a pulmonary artery catheter (PAC) in place. However, unambiguous data in support of this view are scarce, and several studies suggest that bedside pulmonary artery catheterization may not benefit most critically ill patients and in fact may lead to some serious complications (see “Effect of Pulmonary Artery Catheterization on Outcome”).Determinants of Cardiac PerformanceCardiac performance requires the integration of multiple mechanical and physiologic parameters of both the heart itself and of the circulatory system through which


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Surgery_Schwartz. of Cardiac PerformanceCardiac performance requires the integration of multiple mechanical and physiologic parameters of both the heart itself and of the circulatory system through which blood flows. The following sections discuss some of these factors, including preload, contractility, and afterload. A brief review of some of the graphical tools for evaluating cardiac physiology is demon-strated in Fig. 13-2.Preload. Starling’s law of the heart states that the force of muscle contraction depends on the initial length of the cardiac fibers. Using terminology that derives from early experiments using isolated cardiac muscle preparations, preload is the stretch of ventricular myocardial tissue just prior to the next contrac-tion. Strictly speaking, preload is determined by end-diastolic volume (EDV). In practice, EDV is challenging to measure precisely during the cardiac cycle, and so clinicians utilize the end-diastolic pressure (EDP) as a reasonable surrogate. For the right ventricle,


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Surgery_Schwartz. (EDV). In practice, EDV is challenging to measure precisely during the cardiac cycle, and so clinicians utilize the end-diastolic pressure (EDP) as a reasonable surrogate. For the right ventricle, central venous pressure (CVP) approximates right ventricular EDP. For the left ventricle, pulmonary artery occlusion pressure (PAOP), which is measured by transiently inflating a balloon at the end of a pressure monitoring catheter positioned in a small branch of the pulmonary artery, approxi-mates left ventricular EDP. The presence of atrioventricular val-vular stenosis may alter this relationship.There are limits to the utilization of EDP as a surrogate for EDV when evaluating preload. For example, EDP is deter-mined not only by volume but also by the diastolic compliance of the ventricular chamber. Ventricular compliance is altered by Brunicardi_Ch13_p0433-p0452.indd 43622/02/19 2:20 PM 437PHYSIOLOGIC MONITORING OF THE SURGICAL PATIENTCHAPTER 13Figure 13-2 A-D. Left ventricular


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Surgery_Schwartz. chamber. Ventricular compliance is altered by Brunicardi_Ch13_p0433-p0452.indd 43622/02/19 2:20 PM 437PHYSIOLOGIC MONITORING OF THE SURGICAL PATIENTCHAPTER 13Figure 13-2 A-D. Left ventricular pressure-volume loops constructed for various clinically relevant scenarios. For further information refer to the text. A. Standard left ventricular pressure-volume loop, with stroke volume, end systolic volume, and end diastolic volume highlighted for reference. Note the directionality of the pressure-volume loop, which is not annotated in the other figures for clarity. B-D. Demonstration of the effect of changing preload (B), contractility (C), or afterload (D) on the pressure-volume relationships in the left ventricle. Note the differences in stroke volume for various conditions, as well as the end-systolic volume and pressures, as these represent clinically significant parameters that govern patient care.various pathologic conditions and pharmacologic agents. Fur-thermore, the


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Surgery_Schwartz. well as the end-systolic volume and pressures, as these represent clinically significant parameters that govern patient care.various pathologic conditions and pharmacologic agents. Fur-thermore, the relationship between EDP and true preload is not linear, but rather is exponential (Fig. 13-2A,B). This fact limits the utility of EDP as a surrogate marker at extremes of EDV.Contractility. Contractility is defined as the inotropic state of the myocardium. Contractility is said to increase when the force of ventricular contraction increases at constant preload and afterload. Clinically, contractility is difficult to quantify because virtually all of the available measures are dependent to a certain degree on preload and afterload. If pressure-volume loops are constructed for each cardiac cycle, small changes in preload and/or afterload will result in shifts of the point defining the end of systole. These end-systolic points on the pressure-versus-volume diagram describe a straight line,


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Surgery_Schwartz. small changes in preload and/or afterload will result in shifts of the point defining the end of systole. These end-systolic points on the pressure-versus-volume diagram describe a straight line, known as the end-systolic pressure-volume line. A steeper slope of this line indicates greater contractility, as illustrated in Fig. 13-2C.Afterload. Afterload is another term derived from in vitro experiments using isolated strips of cardiac muscle and is defined as the force resisting fiber shortening once systole begins. Defined specifically for the in vivo system, afterload is the resistance to the expulsion of blood from the heart chamber of interest, usually the left ventricle. Several factors comprise the in vivo correlate of ventricular afterload, including ven-tricular chamber geometry, intracavitary pressure generation, and the arterial impedance in the systemic circulation. Since these factors are difficult to assess clinically, afterload is com-monly approximated by calculating


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Surgery_Schwartz. intracavitary pressure generation, and the arterial impedance in the systemic circulation. Since these factors are difficult to assess clinically, afterload is com-monly approximated by calculating systemic vascular resistance (SVR), defined as mean arterial pressure (MAP) divided by car-diac output (Fig. 13-2D).PLACEMENT OF THE PULMONARY ARTERY CATHETERIn its simplest form, the PAC has four channels. One channel terminates in a balloon at the tip of the catheter. The proximal end of this channel is connected to a syringe to permit inflation of the balloon with air. Prior to insertion of the PAC, the integ-rity of the balloon should be verified by inflating it. In order to minimize the risk of vascular or ventricular perforation by the relatively inflexible catheter, it also is important to verify that the inflated balloon extends just beyond the tip of the device. A second channel in the catheter contains wires that are connected Brunicardi_Ch13_p0433-p0452.indd 43722/02/19 2:21


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Surgery_Schwartz. to verify that the inflated balloon extends just beyond the tip of the device. A second channel in the catheter contains wires that are connected Brunicardi_Ch13_p0433-p0452.indd 43722/02/19 2:21 PM 438BASIC CONSIDERATIONSPART Ito a thermistor located near the tip of the catheter. At the proxi-mal end of the PAC, the wires terminate in a fitting that permits connection to appropriate hardware for the calculation of car-diac output using the thermodilution technique. The final two channels are used for pressure monitoring and the injection of the thermal indicator for determinations of cardiac output. One of these channels terminates at the tip of the catheter; the other terminates 20 cm proximal to the tip.Placement of a PAC requires access to the central venous circulation. Such access can be obtained at a variety of sites, including the antecubital, femoral, jugular, and subclavian veins. Percutaneous placement through either the jugular or sub-clavian vein generally is


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Surgery_Schwartz. access can be obtained at a variety of sites, including the antecubital, femoral, jugular, and subclavian veins. Percutaneous placement through either the jugular or sub-clavian vein generally is preferred. Right internal jugular vein cannulation carries the lowest risk of complications, and the path of the catheter from this site into the right atrium is straight. In the event of inadvertent arterial puncture, local pressure is significantly more effective in controlling bleeding from the carotid artery as compared to the subclavian artery. Neverthe-less, it is more difficult to keep occlusive dressings in place on the neck than in the subclavian fossa. Furthermore, the anatomic landmarks in the subclavian position are quite constant, even in patients with anasarca or massive obesity; the subclavian vein is always attached to the deep (concave) surface of the clavicle. In contrast, the appropriate landmarks to guide jugular venous cannulation are sometimes difficult to discern in


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Surgery_Schwartz. the subclavian vein is always attached to the deep (concave) surface of the clavicle. In contrast, the appropriate landmarks to guide jugular venous cannulation are sometimes difficult to discern in obese or very edematous patients. However, ultrasonic guidance, which should be used routinely, has been shown to facilitate bedside jugular venipuncture.14Cannulation of the vein is normally performed percuta-neously, using the Seldinger technique. A small-bore needle is inserted through the skin and subcutaneous tissue into the vein. After documenting return of venous blood, a guidewire with a flexible tip is inserted through the needle into the vein, and the needle is withdrawn. A dilator/introducer sheath is passed over Figure 13-3. Representative pressure traces at different stages of insertion of the PAC. In the central venous circulation, the pressure remains low, with characteristic waves from atrial filling and tricuspid valve closing. Upon entry into the right ventricle, the


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Surgery_Schwartz. insertion of the PAC. In the central venous circulation, the pressure remains low, with characteristic waves from atrial filling and tricuspid valve closing. Upon entry into the right ventricle, the pressure increases sharply, with the broadest range between systole and diastole. When in the main pulmonary artery, the systolic pressure remains elevated to the same degree, but the diastolic pressure is now significantly elevated due to the closure of the pulmonic valve during the cardiac cycle. Upon further advancement with the balloon inflated, the pressure differences become smaller and the magnitude of the mean pressure drops, reflecting an estimate of the left atrial pressure.the wire, and the wire and the dilator are removed. The proxi-mal terminus of the distal port of the PAC is connected through low-compliance tubing to a strain-gauge transducer, and the tubing-catheter system is flushed with fluid. While constantly observing the pressure tracing on a monitor screen, the PAC is


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Surgery_Schwartz. through low-compliance tubing to a strain-gauge transducer, and the tubing-catheter system is flushed with fluid. While constantly observing the pressure tracing on a monitor screen, the PAC is advanced with the balloon deflated until respiratory excur-sions are observed. The balloon is then inflated, and the catheter advanced further, while monitoring pressures sequentially in the right atrium and right ventricle en route to the pulmonary artery. The pressure waveforms for the right atrium, right ventricle, and pulmonary artery are each characteristic (Fig. 13-3). The cath-eter is advanced out the pulmonary artery until a damped tracing indicative of the “wedged” position is obtained. The balloon is then deflated, taking care to ensure that a normal pulmonary arterial tracing is again observed on the monitor; leaving the balloon inflated can increase the risk of pulmonary infarction or perforation of the pulmonary artery. Unnecessary measurements of the pulmonary artery occlusion


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Surgery_Schwartz. observed on the monitor; leaving the balloon inflated can increase the risk of pulmonary infarction or perforation of the pulmonary artery. Unnecessary measurements of the pulmonary artery occlusion pressure are discouraged as rupture of the pulmonary artery may occur.HEMODYNAMIC MEASUREMENTSEven in its simplest embodiment, the PAC is capable of pro-viding clinicians with a remarkable amount of information about the hemodynamic status of patients. Additional informa-tion may be obtained if various modifications of the standard PAC are employed. By combining data obtained through use of the PAC with results obtained by other means (i.e., blood hemoglobin concentration and oxyhemoglobin saturation), derived estimates of systemic oxygen transport and utilization can be calculated. Direct and derived parameters obtainable by bedside pulmonary arterial catheterization, along with sev-eral associated approximate normal ranges, are summarized in Table 13-1.Brunicardi_Ch13_p0433-p0452.indd


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Surgery_Schwartz. derived parameters obtainable by bedside pulmonary arterial catheterization, along with sev-eral associated approximate normal ranges, are summarized in Table 13-1.Brunicardi_Ch13_p0433-p0452.indd 43822/02/19 2:21 PM 439PHYSIOLOGIC MONITORING OF THE SURGICAL PATIENTCHAPTER 13Table 13-1Directly measured and derived hemodynamic data obtainable by bedside pulmonary artery catheterization, with normal associated rangesPARAMETERNORMAL RANGECVP0–6 mmHgPAPVariesPAOP6–12 mmHgSv–O2 (intermittent or continuous)65%–70%QT (intermittent or continuous)4–6 L/minQT* (intermittent or continuous)2.5–3.5 L·min-1·m-2RVEF>55%SV40–80 mLSVR800–1400 dyne·sec·cm-5SVRI1500–2400 dyne·sec·cm-5·m-2PVR100–150 dyne·sec·cm-5PVRI200–400 dyne·sec·cm-5·m-2RVEDVVariableD.O2400–660 mL·min-1·m-2V–O2115–165 mL·min-1·m-2ERVariableQS/QTVariableCVP = mean central venous pressure; D.O2 = systemic oxygen delivery; ER = systemic oxygen extraction ratio; PAOP = pulmonary artery occlusion (wedge) pressure; PAP = pulmonary


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Surgery_Schwartz. = mean central venous pressure; D.O2 = systemic oxygen delivery; ER = systemic oxygen extraction ratio; PAOP = pulmonary artery occlusion (wedge) pressure; PAP = pulmonary artery pressure; PVR = pulmonary vascular resistance; PVRI = pulmonary vascular resistance index; QS/QT = fractional pulmonary venous admixture (shunt fraction); QT = cardiac output; QT* = cardiac output indexed to body surface area (cardiac index); RVEDV = right ventricular end-diastolic volume; RVEF = right ventricular ejection fraction; SV = stroke volume; SVI = stroke volume index; Sv–O2= fractional mixed venous (pulmonary artery) hemoglobin saturation; SVR = systemic vascular resistance; SVRI = systemic vascular resistance index; V–O2 = systemic oxygen utilization.Measurement of Cardiac Output by ThermodilutionBefore the development of the PAC, determining cardiac output (QT) at the bedside required careful measurements of oxygen consumption (Fick method) or spectrophotometric determina-tion of indocyanine


Surgery_Schwartz

Surgery_Schwartz. the development of the PAC, determining cardiac output (QT) at the bedside required careful measurements of oxygen consumption (Fick method) or spectrophotometric determina-tion of indocyanine green dye dilution curves. Measurements of QT using the thermodilution technique are simple and reason-ably accurate. The measurements can be performed repetitively, and the principle is straightforward. If a bolus of an indicator is rapidly and thoroughly mixed with a moving fluid upstream from a detector, then the concentration of the indicator at the detector will increase sharply and then exponentially diminish back to zero. The area under the resulting time-concentration curve is a function of the volume of indicator injected and the flow rate of the moving stream of fluid. Larger volumes of indi-cator result in greater areas under the curve, and faster flow rates of the mixing fluid result in smaller areas under the curve. When QT is measured by thermodilution, the indicator is heat and


Surgery_Schwartz

Surgery_Schwartz. indi-cator result in greater areas under the curve, and faster flow rates of the mixing fluid result in smaller areas under the curve. When QT is measured by thermodilution, the indicator is heat and the detector is a temperature-sensing thermistor at the distal end of the PAC. The relationship used for calculating QT is called the Stewart-Hamilton equation:QVKK(TT)T(t)dtT12BIB=−˛where V is the volume of the indicator injected, TB is the tem-perature of blood (i.e., core body temperature), TI is the tem-perature of the indicator, K1 is a constant that is the function of the specific heats of blood and the indicator, K2 is an empiri-cally derived constant that accounts for several factors (the dead space volume of the catheter, heat lost from the indicator as it traverses the catheter, and the injection rate of the indicator), and ∫TB(t)dt is the area under the time-temperature curve. In clinical practice, the Stewart-Hamilton equation is solved by a microprocessor.Determination of


Surgery_Schwartz

Surgery_Schwartz. and the injection rate of the indicator), and ∫TB(t)dt is the area under the time-temperature curve. In clinical practice, the Stewart-Hamilton equation is solved by a microprocessor.Determination of cardiac output by the thermodilution method is generally quite accurate, although it tends to system-atically overestimate QT at low values. Changes in blood tem-perature and QT during the respiratory cycle can influence the measurement. Therefore, results generally should be recorded as the mean of two or three determinations obtained at random points in the respiratory cycle. Using cold injectate widens the difference between TB and TI and thereby increases signal-to-noise ratio. Nevertheless, most authorities recommend using room temperature injectate (normal saline or 5% dextrose in water) to minimize errors resulting from warming of the fluid as it transferred from its reservoir to a syringe for injection.Technologic innovations have been introduced that per-mit continuous