The Clinical Handbook for Surgical Critical Care The Clinical Handbook for Surgical Critical Care Second Edition Kenneth W Burchard, MD Dartmouth-Hitchcock Medical Center, New Hampshire, USA CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2012 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S Government works Version Date: 20130226 International Standard Book Number-13: 978-1-84214-588-3 (eBook - PDF) This book contains information obtained from authentic and highly regarded sources While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and not 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licenses and registration for a variety of users For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com Dedication This book is dedicated to my wife, Marion, my son, Paul, and all who encounter the evaluation and management of the surgical patient with critical illness Contents The critical care surgeon Shock The circulation 11 Inflammation 53 The critical surgical abdomen 77 The pulmonary system 86 The renal system 125 The gastrointestinal system 149 The nervous system 167 10 The hematopoietic system Index 187 195 Online features Online case studies and multiple-choice questions are available for viewing at our website To access the features, you will need to first register at http://www.informahealthcare.com where, upon completion of the registration process, you will have the necessary login details If you have previously registered, there is no need to register again After you have completed the registration procedure, please type the following link in your Web browser: http://informahealthcare.com/onlinefeatures/9781841849225 The opening page will request your login details and, after signing in, the material will be available for viewing The critical care surgeon While the designation of a specialized hospital site for immediate postoperative care dates back to the early 1940s, the creation of surgical intensive care units with a capacity for days of monitoring and management did not emerge until about two decades later Prompted by the poliomyelitis epidemic of the 1940s, the demand for effective mechanical ventilation resulted in positive pressure ventilators, which became more widely utilized in these new intensive care settings Over the ensuing decades, the initial primacy of airway and breathing support has been equaled by the implementation of monitoring and manipulation of the circulation This has been accompanied by improvements such as better use of blood products, renal replacement therapy, transplant surgery, emergency cardiac interventions, novel anesthetic agents, new antibiotics, etc (1) These advancements have prolonged and saved the lives of patients with surgical critical illness, resulting in not only these better outcomes, but also a monumental effort at clinical and experimental investigation to elucidate the fundamental pathophysiology of these disorders and principles of management Since the beginning of critical care concepts, surgeons have been actively engaged in patient care, education, leadership, and scholarly pursuits linked to surgical critical illness By 1987, the American Board of Surgery recognized that surgeons with a special interest and expertise in surgical critical illness should be acknowledged with subspecialty board certification Since the 1980s, subspecialization within the context of general surgery has become more prevalent with and without subspecialty board certification, especially in academic medical centers (2) Vascular surgery, surgical oncology, colorectal surgery, and minimally invasive surgery, for instance, have become common arenas of expertise with little or no regular exposure to patients with surgical critical illness In contrast, trauma surgery, another common practice of special interest, has maintained an active surgical critical care component with fellowship trainees expected to attain surgical critical care board certification This special qualification of the trauma surgeon combined with infrequent exposure of other general surgery specialties to surgical critical illness has been a principle underpinning to the creation of yet another specialty—the acute care surgeon THE ACUTE CARE SURGEON The acute care surgeon combines the interests and expertise of the trauma surgeon, the critical care surgeon, and the general surgeon who attends “time-sensitive” surgical conditions The expectation that many sociological, training, and practice preference features will demand an increasing workforce of acute care surgeons has resulted in the plan for fellowship training in the specialty of acute care surgery (2–4) Training in surgical critical care is a fundamental component of this new training paradigm, and this manual is designed to assist that training, especially from the perspective that surgical critical illness is, indeed, a surgical condition best understood and manipulated by surgeons THE CRITICAL CARE SURGEON TRAINEE The trainee in surgical critical care characteristically proceeds through three phases in achieving competence in the primary goals of surgical critical care The first phase is exemplified by the question “Where is the hole?” This refers to the early encounters of a trainee (usually first and second year general surgery residents) with a patient who is typically suddenly ill and the trainee’s efforts to define the primary, sometimes life-threatening, organ alteration that needs immediate attention (Table 1.1) For instance, sudden hypotension after major abdominal surgery might prompt questions about hypovolemia, anesthetics, and myocardial infarction THE CLINICAL HANDBOOK FOR SURGICAL CRITICAL CARE Table 1.1 The Surgical Trainee in Critical Care Examples of Question Related Problems Where is the hole? A Hypotension B Respiratory distress C Oliguria D Fever E Mental status change How I plug the hole? A IV fluid B Packed RBCs C Inotropes D Ventilator E Diuretics F Sedatives Why is the hole there? A Bleeding B Infection C Missed intra-abdominal injury D Anastomotic leak E Pulmonary embolism F Myocardial infarction The trainee’s next question is “How I plug the hole?” Asking this, the trainee (usually a second or third year resident) who has decided that the hypotension is from hypovolemia considers the type and amount of intravenous fluid to administer The third question is “Why is the hole there?” This question is best answered when one has knowledge about the surgical disease and surgical procedure This is the principle focus for the education of more senior trainees, especially a surgical critical care or acute care fellow This question frequently drives sophisticated surgical decision making Is there an anastomotic leak? Is there an ischemic left colon? Does this patient need additional surgery? I proffer that answering the question “Why is the hole there?” is the most important determinant of the outcome for critically ill surgical patients THE PRACTICING SURGEON Even in the setting of an elective surgical practice or a nearby acute care surgery institution, every practicing surgeon can be faced with managing disease in keeping with the primary goals of surgical critical care Trauma, intestinal hemorrhage, intestinal perforation, leaking anastomoses, and pancreatitis are common examples of disease states that could provide such a challenge and opportunity The fundamentals of good surgical care—resuscitation of the circulation, debridement of dead tissue, drainage of infection, and minimizing surgical trauma— all diminish the risk of cellular injury, organ malfunction, and the associated morbidity and mortality threats It is often difficult, however, for practicing surgeons to maintain current knowledge of advancements in monitoring and technology, which provide more information and sometimes enhanced management of the “How I plug the hole?” issues of surgical critical care In addition, the practicing surgeon may not encounter critically ill patients with sufficient frequency to recognize immediately how a problem with the circulation or respiration may relate to the underlying surgical disease or procedure Thus, the practicing surgeon may have difficulty answering the question “Why is the hole there?” for some patients THE CLINICAL HANDBOOK FOR SURGICAL CRITICAL CARE The purpose of this handbook is to assist the surgical/critical care trainee and the practicing surgeon with all three questions related to surgical critical care and to emphasize the question THE CRITICAL CARE SURGEON “Why is the hole there?” Since much of surgical critical illness is secondary to shock, this topic will begin the guide and will be given special consideration in each subsequent chapter, as appropriate Shock is the principle “hole” that must be effectively plugged to prevent or diminish cell and organ injury Discerning the etiology of shock becomes linked to a mature understanding of surgical disease and intervention Effective surgical critical care decision making then becomes the principle attribute of the sophisticated practitioner of surgical critical care, an expert in discerning “Why is the hole there?” REFERENCES Richard W, Carlson MAG, ed Principles and Practice of Medical Intensive Care Philadelphia: W.B Saunders Company, 1993 Davis KA, Rozycki GS Acute care surgery in evolution Crit Care Med 2010; 38(9 Suppl): S405–10 Endorf FW, Jurkovich GJ Acute care surgery: a proposed training model for a new specialty within general surgery J Surg Educ 2007; 64: 294–9 Hoyt DB, Kim HD, Barrios C Acute care surgery: a new training and practice model in the United States World J Surg 2008; 32: 1630–5 Shock Those who cannot remember the past are condemned to repeat it —George Santayana (1863–1952) HISTORIC CONCEPTS OF SHOCK From the latter half of the nineteenth century through the twentieth century, the concepts and definitions of shock have been varied and often considered mutually exclusive (Table 2.1) During the first half of the twentieth century, the advocates of hypovolemic hypoperfusion as the principle etiology of shock (e.g., Blalock and Wiggers) vigorously opposed the advocates of circulating toxins as the mechanism (e.g., Cannon) (1–4) As the twenty-first century has proceeded, this same advocacy continues, but the necessity of exclusivity has dissipated The concept of shock that will be emphasized in The Clinical Handbook for Surgical Critical Care also has a historic underpinning In 1872, Samuel D Gross offered the analysis that during shock “ the machinery of life has been rudely unhinged ”—a formulation that allows for a coalescence of etiologies rather than strict separation (5) Today, shock can be considered a manifestation of total body cell metabolic disturbance— an unhinging of life machinery most vigorously manifested by decreased total body oxygen consumption The principle etiologies of this alteration are still connected to the twentiethcentury debate Too little oxygen delivery and too much inflammatory toxin both are capable of producing shock In fact, these two processes are not mutually exclusive, but are characteristically additive threats to cell function Simply stated, hypoperfusion begets inflammation, and inflammation begets hypoperfusion (Table 2.2) Shock from severe hypoperfusion and severe systemic inflammation is the cause of death and/or multisystem organ failure in surgical critical illness Understanding these mechanisms of cell metabolic threat can augment all features of surgical critical care evaluation and management (Where is the hole? How I plug the hole? Why is the hole there?) Therefore, repeating the history of shock concepts from Gross through Cannon, Blalock and Wiggers to more modern contributors like Gann and Rivers can prove more a reward than a condemnation (6,7) SHOCK AND DECREASED OXYGEN UTILIZATION Decreased Oxygen Delivery Oxidative phosphorylation is the primary metabolic process whereby mammalian cells produce cellular energy and heat Ninety percent of oxygen utilization occurs in the mitochondria and ATP production accounts for 80% of oxygen consumption (8) While deficits in arterial oxygen saturation and blood hemoglobin concentrations can limit oxygen delivery to cells, most often a reduction in blood flow (hypoperfusion) is responsible for diminished oxidative phosphorylation When total body oxygen delivery is sufficiently compromised, total body oxygen consumption must decrease, a condition termed “delivery-dependent oxygen consumption” Figure 2.1, (9) The inflection point where the increasing consumption curve levels off has been termed as the “critical” oxygen delivery state of that preparation Oxygen consumption that is delivery dependent and below critical is associated with evidence of cellular energy deficits (e.g., lactic acidosis and hypothermia) (10,11) In 1942, Cuthbertson described metabolic alterations following tissue injury and linked the combination of hypothermia and decreased oxygen consumption to a reduction in cell vitality, which he termed as the “Ebb Period” or “Ebb Phase.” Most of The Ebb Period was secondary to “tissue asphyxia” and associated with a high mortality rate (12,13) When minute by minute oxygen delivery is insufficient to meet oxidative phosphorylation demands, this is termed an oxygen deficit When the deficit continues over many minutes, then the product of deficit and minutes is termed as the oxygen debt Global hypovolemic hypoperfusion (decreased cardiac output from decreased intravascular volume) is the most A B C D E Prolonged PEEP effect Decreased systemic mediator concentrations Decreased lung water accumulation Improved venous oxygenation Improved acid-base status ANS: D A 24-year-old male is in the intensive care unit 12 hours after a motorcycle crash that resulted in bilateral hemopneumothorax, bilateral rib fractures, and bilateral pulmonary contusions (see the radiograph below) No other injuries were identified Three days later his pO2/FiO2 has improved from 90 to 200 The left pulmonary infiltrates are much less dense, but the right lung density is unchanged The most likely reason for lack of resolution of the right lung infiltrate is: A B C D E Pulmonary hemorrhage Unrecognized right flail chest Undrained hemothorax Pulmonary infarction Nosocomial infection ANS: E The renal system – Multiple choice questions A 55-year-old man fell from a scaffold, which was toppled by a large concrete block as it fell from a crane His left leg was pinned under the concrete After extrication, his leg below the knee was pale and motionless with moderate pain The patient was transported to your emergency room with a blood pressure of 100/60 mm Hg, pulse 120 bpm, temperature 37.5°C, and respirations of 25/min noted on admission Insertion of a Foley catheter revealed dark brown colored urine EKG monitoring revealed peaked T waves Serum electrolytes were Na 142 meq/L, K 6.8 meq/L, Cl 106 meq/L, TCO2 18 meq/L Serum BUN mg/dL was 25, creatinine 2.0 mg/dL His ionized calcium is 0.90 mmol/L (normal 1.15– 1.33 mmol/L) The principal cause of this man’s acute kidney injury is: A B C D E Hypocalcemia Hypotension Rhabdomyolysis Hyperkalemia Systemic inflammation ANS: C A 45-year-old man with previously known duodenal ulcer disease presents with complaints of persistent vomiting for the past 36 hours The vomit is clear-looking and acidic in taste Prior to the vomiting he had difficulty with solid foods causing “fullness” in the stomach and he had been taking only liquids for one week Antacids have not helped and he did not seek medical attention until today He complains of being dizzy when he stands up His blood pressure changes from 120/70 when lying to 105/55 when standing, his pulse changes from 100 to 130 Which intravenous fluid plan will best alleviate his intravascular volume and acid-base disturbance? A B C D E Three liters of 0.9% saline with 40 meq of potassium per liter Three liters of lactated Ringer’s solution Two liters of D5 + 0.45% saline with 40 meq of potassium per liter Two liters of lactated Ringer’s solution with 30 meq potassium per liter Three liters of D5+ W with 40 meq of potassium per liter ANS: A An un-helmeted 18-year-old male was in a motorcycle accident He suffered a severe closed head injury with diffuse axonal injury He remains comatose three days later with fever (38.5°C–40°C) and is noted to have urine output of 500 cm3/hr The specific gravity of the urine is 1.004 and his serum electrolytes demonstrate: sodium 155 meq/L; chloride 125 meq/L; potassium 4.5 meq/L; TCO2 25 meq/L The principal reason for these electrolyte findings is: A B C D E Increased aldosterone secretion Increased cortisol secretion Decreased vasopressin secretion Evaporative water loss Decreased B-type natriuretic peptide secretion ANS: C A 65-year-old man with known hypertension (usual systolic 150 mm Hg – use of beta blocker and ASE inhibitor therapy) and congestive heart failure (ejection fraction of 35%— use of diuretics) is in the Intensive Care Unit 12 hours after surgery for a perforated duodenal ulcer For the past four hours, his urine output has been 15–20 cm3/hr He has sequestered 10 L of fluid and gained kg in weight since Emergency Department arrival His blood pressure is 110/60 mm Hg and his pulse is 100 bpm He remains intubated and with a FiO2 of 30% his oxygen saturation is 98% His bladder catheter is patent and his urine indices demonstrate a FeNa of 0.3% Which of the following parameters is most indicative of the etiology of his oliguria: A B C D E His input and output calculation His body weight measurement His oxygenation status His pulse His blood pressure ANS: E A 22-year-old unrestrained driver in a motor vehicle crash arrives at a Level Trauma Center with the following parameters: blood pressure 80/60 mm Hg, pulse 130 bpm, respirations 28/min, and temperature 36°C He is intubated for altered mental status and undergoes left chest closed thoracostomy for a hemopneumothorax He is administered four liters of lactated Ringer’s solution through a rapid infusion, fluid warming device A FAST scan is positive for fluid in the abdomen, and as he arrives in the operating room, the following data are provided: arterial pH 7.22, arterial pCO2 32 mm Hg, arterial pO2 150 mm Hg, ionized calcium 0.90 mmol/L (normal 1.15–1.33 mmol/L) The principal reason for his low ionized calcium is: A B C D E Hypothermia Hypovolemic hypoperfusion Lactated Ringer’s infusion Metabolic acidosis Hyperventilation ANS: B The gastrointestinal system – Multiple choice questions A 52-year-old man with known alcoholic liver disease comes to the hospital because of increasing abdominal distention Physical exam demonstrates abdominal distention with dilated subcutaneous veins There is tympany in the anterior abdomen and dullness in both flanks An ultrasound study of the abdomen shows fluid The principal cause of ascites in alcoholic liver disease is: A B C D E Decreased serum oncotic pressure Intrahepatic sinusoidal obstruction Increased right atrial pressure Hepatic vein sclerosis Obstruction of intestinal lymph drainage ANS: B Primary peritonitis can be best differentiated from secondary peritonitis by which of the following: A B C D E The patient’s hemodynamics The patient’s renal function The white blood count in ascites fluid The MELD score The microbiology of ascites ANS: E A 36-year-old male alcoholic is admitted to the Intensive Care Unit with acute pancreatitis His blood pressure is 100/60 mm Hg, pulse 110 bpm, respirations 28/min, oxygen saturation 92% on a 50% face mask, and temperature 38.6°C His hemoglobin is 17.2 gm/dl His ionized calcium is 1.00 mmol/L (normal 1.15–1.33 mmol/L) His central venous saturation is 55% and his lactic acid is 3.6 mmol/L His abdominal pressure is 15 mm Hg The most likely reason for his circulation status is: A B C D E A plasma volume deficit Myocardial depressants Hypocalcemia Metabolic acidosis Abdominal compartment syndrome ANS: A A 72-year-old female received a seven day course of ciprofloxacin for a urinary tract infection two weeks ago For the past three days she has developed progressively increasing diarrhea Her vital signs are: Temperature 38.6°C, BP 100/60 mm Hg, pulse 110 bpm, respirations 28/min, oxygen saturation 98% on L/min of nasal oxygen She is agitated and delirious Her abdomen is distended with hyperactive bowel sounds, tympanic to percussion, and tender only to deep palpation in the left lower quadrant Rectal exam shows liquid, foul smelling stool, no blood, and no masses A plain abdominal radiograph shows thickened descending and sigmoid colonic walls as well as thumbprinting Her laboratory data are: hemoglobin 15.5 gm/dl, WBC 24,000/mm3, BUN 35 mg/dl, creatinine 1.5 mg/dl, bicarbonate 18 meq/L The most likely diagnosis is: A B C D E Ischemic colitis Ulcerative colitis Salmonella colitis Crohn’s colitis Clostridium difficile colitis ANS: E A 28-year-old male is in the intensive care unit 10 days after a gunshot wound to the abdomen that resulted in injury to the stomach, the distal transverse colon, the spleen and the tail of the pancreas At surgery, he underwent repair of the stomach, splenectomy, distal pancreatectomy, colectomy, and formation of a right transverse colostomy His postoperative course has been marked by continuing fever, tachycardia, and leukocytosis Drains placed at the time of surgery have been supplemented by percutaneous drainage of purulent collections that have grown Escherichia coli and Bacteroides Glucose elevation has been managed with insulin (20–30 units/day) and his pre-albumin has been 8–10 mg/dl (normal 20–40 mg/dl) despite the initiation of intestinal feeding on POD A nitrogen balance study on POD shows a loss of g in 24 hours The protein-rich site that has suffered the greatest loss of body cell mass is: A B C D E Skeletal muscle Liver Heart Intestine Kidneys ANS: A The nervous system – Multiple choice questions A 24-year-old un-helmeted motorcycle crash driver is brought to the Emergency Department 30 minutes after EMT arrival He was intubated at the scene for a GCS of Once intubated, his ABCs were satisfactory and remain so in the trauma bay Physical exam shows: a right pupil that is larger and less reactive than the left; a right corneal reflex that is absent; he extends his left arm and leg to noxious stimuli; he withdraws his right arm and leg to noxious stimuli Which of the following traumatic brain injury diagnosis is most likely? A B C D E Diffuse axonal injury Subarachnoid hemorrhage Frontal lobe intraparenchymal hemorrhage Subdural hemorrhage Brain stem contusion ANS: D A 66-year-old insulin-dependent diabetic woman is noted to be suddenly unresponsive She is in the hospital for staphylococcal bacteremia Her blood pressure is 140/90 mm Hg, pulse 90 bpm, respirations 18/min, and her oxygen saturation is 96% on room air Examination shows brisk pupillary constriction and dilation, brisk corneal reflexes, and normal oculo-vestibular reflexes Noxious stimuli result in symmetrical withdrawal of the upper and lower extremities The most likely reason for her altered mental status is: A B C D E Brainstem basilar artery infarct Depressed cortical metabolism Left middle cerebral artery stroke Meningitis Subarachnoid hemorrhage ANS: B An 18-year-old female is the back seat passenger in a motor vehicle crash who suffered bilateral cerebral contusions associated with a GCS of 13 on admission to the Emergency Department Reportedly, she had no loss of consciousness No other injuries are identified Twelve hours later, her respiratory rate has increased from the 12–14 range to the mid 20s Her oxygen saturation on room air has decreased from 95% to 85% and a chest radiograph shows bilateral infiltrates, most prominent in the hilar region She has received two liters of isotonic crystalloid since admission and has made 400 cm3 of urine The most likely etiology of her respiratory status is: A B C D E Bilateral aspiration Bilateral pulmonary contusion Neurogenic pulmonary edema Stunned myocardium Community acquired pneumonia ANS: C A 44-year-old unrestrained driver in a motor vehicle crash is comatose in the Intensive Care Unit two days after the event that resulted in diffuse axonal injury His intracranial pressure (ICP) has most often been in the 20–25 mm Hg range, and he is receiving vasoconstrictor infusion to maintain a cerebral perfusion pressure greater than 60 mm Hg Fluid management that might assist attempts to lower the ICP is: A B C D E Diuretic administration Albumin administration Lactated Ringer’s administration Hypertonic saline administration Fluid restriction to 500 cm3/day ANS: D The hematopoietic system – Multiple choice questions A 24-year-old man is three days post emergency splenectomy for a ruptured spleen At the time of his abdominal surgery, orthopedics placed an external fixator on a comminuted, left tibia-fibula fracture Orthopedics plans internal fixation tomorrow and because his hemoglobin is 6.8 gm/dl, he receives two units of crossmatched red blood cells Thirty minutes after the second unit, his temperature increases from 37.6°°C to 38.9°°C His respiratory rate has increased from 16–18/min to 22–26/min His oxygen saturation has remained 96% on two liters of nasal oxygen The most likely reason for this temperature elevation is: A B C D E ABO incompatibility Bacterial contamination Acute lung injury Alloimmunization from transfused leukocytes Interleukin-6 in the transfusion ANS: D A 55-year-old female has undergone emergency sigmoid resection, colostomy, and Hartman’s pouch formation for perforated diverticulitis During the surgery, persistent hypotension was addressed by the administration of eight liters of isotonic crystalloid and vasopressin She is now in the intensive care unit four hours after surgery Her MAP on vasopressin is 65 mm Hg, her central venous pressure is 15 mm Hg, and her central venous oxygen saturation is 58% Her lactic acid blood concentration was 3.6 mmol/L during the surgery and has increased to 4.4 mmol/L Her hemoglobin is 7.2 gm/dl The next step in goal-directed resuscitation for this woman with sepsis is: A B C D E Administration of three liters of lactated Ringer’s solution over 15 minutes Discontinuation of vasopressin Administration of three units of packed red cells Administration of dopamine 5–10 μg/kg/min Administration of norepinephrine 8–12 μg/min ANS: C The principal reason for coagulopathy associated with massive transfusion is: A B C D E Dilution of coagulation factors Administration of stored blood Hypocalcemia Poor metabolism of citrate Tissue injury ANS: E Which of the following sites of injury is most likely to result in a hypocoagulation state? A B C D E Pulmonary contusion Traumatic brain injury Liver injury Femur fracture Ruptured bladder ANS: B A 48-year-old female has been in the intensive care unit for eight days following surgery for ischemic bowel secondary to an embolism to her superior mesenteric artery She has been receiving full dose unfractionated heparin to maintain a PTT in the 60–80–second range Today her platelet count is noted to be 70,000/mm3, a drop from 150,000/cmm two days ago The intravenous catheter on her left arm has become nonfunctional and there is a tender subcutaneous cord extending cephalad from the intravenous insertion site A diagnosis of heparin induced thrombocytopenia is supported best by which of the following: A B C D E Detection of heparin associated antibody Thrombocytopenia during unfractionated heparin infusion Previous diagnosis of thrombo-embolic event Detection of a DVT in a lower extremity A 4T score of ANS: E Index AAC See Acute acalculous cholecystitis Abdominal compartment syndrome (ACS) diagnosis, 80–81 etiologies, 79–80 pathophysiology, 79–80 Abdominal distention, 65 Abdominal examination, pathological inflammation, 65 Abdominal perfusion pressure (APP), 79, 81 Abdominal pressure hemodynamic monitoring, 40 increased, 40 Abdominal viscera and damage control laparotomy, 83 management, 82–84 ABG See Arterial blood gas Abscess, intra-abdominal, 159–160 Acid-base monitoring, 24 Acid–base physiology, 136–139 Acidosis, 77 metabolic, 138 ACS See Abdominal compartment syndrome Acute acalculous cholecystitis (AAC), 153–154 Acute care surgeon, Acute kidney injury (AKI) definition, 127 epidemiology, 131 hemodynamic management, 131 history and physical examination, 127–128 inflammation management, 131–132 laboratory investigation, 128–130 pathophysiology, 130 renal replacement, 132–133 Acute lung injury (ALI) AECC definitions, 100 diagnosis, 101–102 management, 102–104 systemic mediators, 100 TBI-associated organ malfunction, 181 Acute pancreatitis augmented systemic inflammation, 156 etiologies, 155 gallstone pancreatitis, 157 hypoperfusion, 154–155 infectious complications, 156 inflammation, 156 nutrition, 156 Acute respiratory distress syndrome (ARDS) AECC definitions, 100 diagnosis, 101–102 differentiation, 101 management, 102–104 systemic mediators, 100 Adrenal insufficiency, 143–144 AECC See American-European Consensus Conference Airway pressure, 92–94 Airway resistance, 91 Alarmins, 57 Alcohol-induced cirrhosis, 153 Alkalosis, metabolic 138–9 ALI See Acute lung injury Alveolar pressure (Palv), 93 Alveolar ventilation, 86 American Board of Surgery, American-European Consensus Conference (AECC), 99 Anion gap, metabolic acidosis 138 ANP See Atrial natriuretic peptide Antibiotic therapy, 160 APP See Abdominal perfusion pressure ARDS See Acute respiratory distress syndrome Arrhythmias, 45 Arterial blood gas (ABG), 98 Arterial lines complications, 28 indications for hemodynamic monitoring, 29 Arterial pressure measurement, 20 Arterial vascular resistance, 15 Ascites, 153 Atrial natriuretic peptide (ANP), 127 Augmented systemic inflammation, 156 Auto-PEEP See Auto-positive end-expiratory pressure Auto-positive end-expiratory pressure (Auto-PEEP), 115 Basilar skull fracture, 178 BCVI See Blunt cerebrovascular injury Beta-blocker (BB) therapy, 180 Biliary tree 151–154 Blood flow, 11 Blood urea nitrogen (BUN), 129 Blood volume measurement, 21 Bloody vicious cycle, 77 Blunt cerebrovascular injury (BCVI), 182–183 Blunt trauma cardiac injury, 106 BNP See B-type natriuretic peptide Body fluid compartments, 133 Brain function hypoperfusion effects, 171–172 inflammation effects, 172–173 physical examination of patient, 173–174 Brain injury See Traumatic brain injury Brain oxygenation, 179–180 Brainstem, 167 B-type natriuretic peptide (BNP), 127 BUN See Blood urea nitrogen Carbon dioxide, dissociation curves 89 Cardiac complication risk, Goldman’s index 30 Cardiac function curve, 14 Cardiac output measurement confounding variables, 27–28 hemodynamic monitoring esophageal Doppler monitor, 22 thermodilution, 21–22 ultrasound, 22 Cardiac trauma, 47 Cardiogenic hypoperfusion cardiogenic shock etiologies, 44 laboratory aids, 45 physical examination, 44 treatment, 45 196 Cardiogenic hypoperfusion (Continued) congestive heart failure etiologies, 41 laboratory aids, 42–43 physical examination, 41–42 treatment, 43–44 Cardiogenic shock etiologies, 44 laboratory aids, 45 physical examination, 44 treatment, 45 Cardiovascular drugs diuretics, 32 inotropic agents, 31–32 vasodilator therapy, 32 vasopressor agents, 31 Cardiovascular system hemodynamic monitoring acid-base monitoring, 24 arterial pressure measurement, 20 blood volume measurement, 21 cardiac output measurement, 21–22 continuous electrocardiogram monitoring, 20 mixed venous oxygen saturation measurement, 23–24 oxygen delivery and consumption measurement, 23 purpose of, 19–20 tissue oxygen measurement, 22–23 tissue pCO2 measurement, 23 venous pressure measurement, 20–21 physical examination regional perfusion, 19 total body perfusion, 17–19 right and left ventricles, 15 vascular resistance, 15–16 venous return description of, 16–17 factors altering, 18 ventricular physiology, 12, 15 CBF See Cerebral blood flow CCV See Critical closing volume CDAD See Clostridium difficile associated disease Central nervous system (CNS) anatomy, 167 coma, 173 hypoperfusion effects, 171–172 inflammation effects, 172–173 malfunction basilar skull fracture, 178 blunt cerebrovascular injury, 182–183 brain oxygenation, 179–180 head trauma, 174–176 intracranial pressure, 179–180 neuromuscular disorder, 183 spinal cord injury, 182–183 symmetrical downward brainstem displacement, 178 temporal lobe herniation, 177 traumatic brain injury, 180–184 physical examination of patient, 173–174 physiology, 167–171 Cerebral blood flow (CBF), 167–168 Cerebral metabolic rate of oxygen (CMRO2), 167–168 Cerebral perfusion pressure (CPP), 168–171, 179–180 Chest radiography, 97 Chest trauma, 104–106 INDEX CHF See Congestive heart failure Child’s criteria, liver disease 152–153 Circulation, 11–48 deficits, 58–60 renal, 125 Clostridium difficile associated disease (CDAD), 157–158 CMV See Controlled mechanical ventilation Coagulation disorders hematopoietic system hypercoagulation, 190–192 hypocoagulation, 189–190 TBI-associated organ malfunction, 181 Coagulopathy, 77 Colloid solutions, 39 Coma, 173 Common ventilator modes (CVM), 115–116 Compliance, 90–92 Confounding variables arterial pressure monitoring, 24–25 cardiac output measurements, 27–28 cardiovascular drugs diuretics, 32 inotropic agents, 31–32 vasodilator therapy, 32 vasopressor agents, 31 complications arterial lines, 28 venous lines, 28–29 indications for hemodynamic monitoring, 29–31 lactic acid, 28 physical examination, 24 urine output, 28 venous pressure monitoring diminished ventricular compliance, 27 disregarding unphysiologic relationship, 26 increased intrathoracic pressure, 27 lack of recognition of proper wave form, 25–26 Congestive heart failure (CHF) etiologies, 41 laboratory aids, 42–43 physical examination, 41–42 treatment, 43–44 Continuous electrocardiogram monitoring, 20 Continuous renal replacement therapy (CRRT), 133 Contractility, 12 Controlled mechanical ventilation (CMV), 93 CPP See Cerebral perfusion pressure Creatinine and urine electrolytes, 129 blood urea nitrogen, 129 Critical care surgeon acute care surgeon, practicing surgeon, trainee, 1–2 Critical closing volume (CCV), 86 Critical surgical abdomen abdominal compartment syndrome damage control laparotomy components, 78–79 damage control resuscitation, 77–78 definition, 77 CRRT See Continuous renal replacement therapy Crystalloid solutions, 38 CT See Total compliance CVM See Common ventilator modes Cytopathic hypoxia, 5–6 INDEX DAD See Diffuse alveolar damage Damage control laparotomy (DCL) components, 78–79 damage control resuscitation, 77–78 Damage control orthopedics (DCO), 184 Damage control resuscitation (DCR), 77–78 DCL See Damage control laparotomy DCO See Damage control orthopedics DCR See Damage control resuscitation Dead space (VD), 86 Deep venous thrombosis (DVT) diagnosis, 110 pulmonary embolism prophylaxis, 112 risk factors, 110 Delivery-dependent oxygen consumption, 4–5 Diabetes insipidus, 181 Dialysis, 132–133 Diarrhea, 157–159 DIC See Disseminated intravascular coagulation Diffuse alveolar damage (DAD), 99–100 Diffusion, 11 2, 3-Diphosphoglycerate (DPG), 11 Disseminated intravascular coagulation (DIC), 189 Distending pressure (DP), 16 Diuretics, 32 DP See Distending pressure DPG See 2, 3-Diphosphoglycerate Duodenum and stomach, 151 DVT See Deep venous thrombosis Ebb phase, 7–8 Echocardiography, 22 Edema, pulmonary, 95 EDM See Esophageal Doppler monitor Elastance, 90–91 Electrocardiogram monitoring, continuous, 20 Electrolyte abnormalities, renal system hyperkalemia, 141–142 hypernatremia, 140–141 hypokalemia, 141 hypomagnesemia, 142 hyponatremia, 140 osmolarity, 142–143 Empyema, 106–109 Enteral feeding, 104 Enteric fistula, 83–84 Esophageal Doppler monitor (EDM), 22 Esophageal hemorrhage, 149, 151 Fat, 61 FFP See Fresh frozen plasma Fibroblasts, 53–54 Flail chest, 104 Flow phase, Fluid overload, 101 Fluid therapy approach for, 134–136 monitoring, 136 reasons for administration, 133–134 Frank–Starling mechanism, 12, 14 FRC See Functional residual capacity Fresh frozen plasma (FFP), 38 Functional residual capacity (FRC), 86 Gallstone pancreatitis, 157 Gastrointestinal disease states acute pancreatitis, 154–157 197 esophageal hemorrhage, 149, 151 intra-abdominal abscess, 159–160 liver and biliary tree, 151–154 small bowel and colon, 157–159 stomach and duodenum, 151 surgical nutrition, 161–162 tertiary peritonitis, 160–161 Gastrointestinal tract (GIT) perfusion, 23 GCS See Glasgow Coma Scale Glasgow Coma Scale (GCS), 172 Global hypovolemic hypoperfusion, 4–5 Glomerular filtration, 125 Goldman cardiac risk index, 30 Head trauma, 174–176 Heart rate, 15 Hematopoietic system coagulation disorders hypercoagulation, 190–192 hypocoagulation, 189–190 massive transfusion in trauma, 187, 189 submassive transfusion, 187 Hemodialysis, 132 Hemodynamic effect inotropic agents, 31 vasodilators, 32 vasopressor drugs, 31 Hemodynamic monitoring acid-base monitoring, 24 arterial pressure measurement, 20 blood volume measurement, 21 cardiac output measurement, 21–22 continuous electrocardiogram monitoring, 20 indications arterial lines, 29 esophageal Doppler monitor, 31 venous lines, 29–30 mixed venous oxygen saturation measurement, 23–24 oxygen delivery and consumption measurement, 23 purpose of, 19–20 tissue oxygen measurement, 22–23 tissue pCO2 measurement, 23 venous pressure measurement, 20–21 Hemofiltration, continuous, 132–133 Hemorrhage, esophageal, 149, 151 Hemorrhagic shock cardiovascular effects, 37 cellular effects, 37 Henderson−Hasselbalch equation, 136–137 Heparin-induced thrombocytopenia (HIT), 189 Hepatorenal syndrome (HRS), 152–153 HFOV See High-frequency oscillatory ventilation High-frequency oscillatory ventilation (HFOV), 119 HIT See Heparin-induced thrombocytopenia Host-defense deficits, 63 Host-defense mechanisms, 54–57 HRS See Hepatorenal syndrome HTS See Hypertonic saline Hypercoagulation, 190–192 Hyperkalemia, 141–142 Hypernatremia, 140–141 Hypertonic saline (HTS), 68 Hypoadrenalism in renal system, 143–144 TBI-associated organ malfunction, 182 INDEX 198 Hypocalcemia, 144–145 Hypocoagulation, 189–190 Hypokalemia, 141 Hypomagnesemia, 142 Hyponatremia, 140 Hypoperfusion acute pancreatitis, 154–155 cardiac trauma, 47 central nervous system, 171–172 clinical diagnosis, 33–34 decreased ionized calcium, 36 etiologies cardiogenic shock, 44–45 congestive heart failure, 41–44 hypovolemia, 36–39 increased abdominal pressure, 40 PEEP, 40 pericardial tamponade, 39–40 tension pneumothorax, 40 gastrointestinal pathophysiology, 149 inflammation effects, 33 metabolic acidosis evidenses, 34 neurohumoral responses, 32 oxygen delivery and consumption, 34–35 pathophysiology, 32 pathophysiology of AKI, 130 postoperative major vascular surgery, 46 postoperative open heart, 45–46 Hypotension See also Cardiogenic shock orthostatic, 17 permissive, 77–78 Hypothermia, management of, 78 Hypovolemia etiologies, 36–37 metabolic/toxic phenomena, 37 physical examination, 37 treatment, 37–39 IABP See Intra-aortic balloon pump IAH See Intra-abdominal hypertension ICP See Intracranial pressure Immunologic enhancement, 70–71 Inflammation acute pancreatitis, 156 central nervous system, 172–173 gastrointestinal pathophysiology, 149 local process host-defense mechanisms, 54–57 stimulants to host-defense responses, 57–58 wound healing, 53–54 metabolic and hormonal responses carbohydrate, 54–57, 60–61 fat, 61 mediators, 62–63 protein, 61 pathophysiology of AKI, 130 severe systemic clinical diagnosis, 64 laboratory studies, 65–66 patient at risk, 64 physical examination, 64–65 severity markers, 66–67 treatment, 67–71 systemic circulation deficits, 58–60 excess inflammatory toxins, 60 and host-defense deficits, 63 Inflammation-induced gastrointestinal tract alterations, 150 Inotropic agents, 31–32 Intra-abdominal abscess, 159–160 Intra-abdominal hypertension (IAH) grading, 79 management, 81 Intra-aortic balloon pump (IABP), 45 Intracranial pressure (ICP), 171, 179–180 Ionized calcium, 36, 66 Jaundice, 151–152 Lactic acid, 24 Liver, 151–154 biliary tree, 151–154 Liver disease, Child’s criteria, 152–153 LMWH See Low-molecular-weight heparin Local inflammation host-defense mechanisms, 54–57 stimulants to host-defense responses, 57–58 wound healing, 53–54 Low-molecular-weight heparin (LMWH), 113 Lung dysfunction acute lung injury diagnosis, 101–102 management, 102–104 systemic mediators, 100 acute respiratory distress syndrome diagnosis, 101–102 differentiation, 101 management, 102–104 systemic mediators, 100 chest trauma, 104–106 empyema, 106–109 hypoperfusion effects, 98 mechanical ventilation, 113–119 pneumonia, 106–109 pulmonary embolism, 109–113 systemic inflammation effects, 98–101 Lung volumes airway pressures, 92–94 alveolar ventilation, 86 arterial PCO2 and PO2 determinants, 86–90 compliance, 90–92 dead space, 86 elastance, 90–91 muscle of respiration, 90 pulmonary fluid, 94–96 pulmonary mechanics, 90 pulmonary monitoring arterial blood gas and saturation, 98 chest radiography, 97 history and physical examination, 96 resistance, 91 work of breathing, 94 Lymphocytes, 53 Mallory–Weiss tear hemorrhage, 151 Massive transfusion (MT), 187, 189 MCFP See Mean circulatory filling pressure Mean airway pressure (Paw), 93 Mean circulatory filling pressure (MCFP), 17 Mechanical ventilation See Ventilation, mechanical Metabolic acidosis, 138 Metabolic alkalosis, 138–139 MODS See Multiple organ dysfunction syndrome INDEX MOF See Multiple organ failure MT See Massive transfusion Multiple organ dysfunction syndrome (MODS), Multiple organ failure (MOF), Muscle of respiration, 90 Myocardial contractility, factors affecting, 14 Myocardial depression, 60, 65 Myocardial dysfunction, 182 Natriuretic peptides, 41 Neuromuscular disorder, 183 Ocular reflexes, unconscious patients, 176 Open abdomen (OA) indications, 81 management, 81–82 Orthostatic hypotension, 17 Osmolarity, 142–143 Osmotic diarrhea, 159 Oxidative phosphorylation, Oxidative stress definition, 57 molecules, 58 Oxygen debt, Oxygen deficit, Oxygen delivery blood flow, 11 decreased, 4–5 diffusion, 11 increased, Palv See Alveolar pressure Pancreatitis acute, 154–156 gallstone, 157 severe acute, 154–156 Ranson’s criteria, 155 Paw See Mean airway pressure Peak inspiratory pressure (PIP), 93 PEEP See Positive pressure at the end of expiration Pericardial tamponade, 39–40 Peritoneal dialysis, 133 Permissive hypotension, 77–78 PIP See Peak inspiratory pressure Plateau pressure (Pplat), 93 Pleural pressure (Ppl), 93–94, 118 PMNs See Polymorphonuclear cells Pneumonia, 106–109 Polymorphonuclear cells (PMNs), 53 Positive pressure at the end of expiration (PEEP), 40, 94 Postoperative major vascular surgery hypoperfusion, 46 Postoperative open heart hypoperfusion, 45–46 Ppl See Pleural pressure Pplat See Plateau pressure Practicing surgeon, Preload, 12 Pressure support ventilation (PSV), 116 Prone ventilation, 118 Protective ventilator management, 117–118 PSV See Pressure support ventilation Ptrans See Transpulmonary pressure Pulmonary artery occlusion pressure (PAOP), 26–27 Pulmonary contusion, 105 Pulmonary edema, 95 Pulmonary embolism, 109–113 Pulmonary fluid, 94–96 199 Pulmonary mechanics components, 90 formulae, 91 Pulmonary monitoring arterial blood gas and saturation, 98 chest radiography, 97 history and physical examination, 96 Pulmonary system acute lung injury, 100–104 acute respiratory distress syndrome, 100–104 airway pressures, 92–94 alveolar ventilation, 86 arterial PCO2 and PO2 determinants, 86–90 chest trauma, 104–106 compliance/elastance, 90–92 dead space, 86 empyema, 106–109 hypoperfusion effects, 98 mechanical ventilation, 113–119 muscle of respiration, 90 pneumonia, 106–109 pulmonary embolism, 109–113 pulmonary fluid, 94–96 pulmonary mechanics, 90 pulmonary monitoring, 96–98 systemic inflammation effects, 98–101 Ranson’s criteria, 154–155 RAS See Reticular activating system Reabsorption sodium, 125–126 tubular, 125 water, 127 Red cell transfusion, 188 Regional hypoperfusion, 80 Regional perfusion, 19 Renal circulation, 125 Renal failure adrenal insufficiency, 143 hemodynamic management, 131 hypomagnesemia, 142 metabolic disturbances, 143–145 Renal function, monitoring, 127 Renal replacement techniques 132–133 Renal system electrolyte abnormalities hyperkalemia, 141–142 hypernatremia, 140–141 hypokalemia, 141 hypomagnesemia, 142 hyponatremia, 140 osmolarity, 142–143 fluid acid–base physiology, 136–139 body fluid compartments, 133 therapy, 133–136 metabolic disturbances hypocalcemia, 144–145 surgical critical illness hypoadrenalism, 143–144 physiology acute kidney injury, 127–133 glomerular filtration, 125 monitoring of renal function, 127 renal circulation, 125 sodium reabsorption, 125–126 tubular reabsorption, 125 water reabsorption, 127 INDEX 200 Reperfusion, 57–58 Resistance, 91 Respiration, muscles, 90 Resuscitation, 47–48 Reticular activating system (RAS) 167 SAP See Severe acute pancreatitis Serum creatinine, 129 See also Creatinine Serum osmolarity, 142 Severe acute pancreatitis (SAP), 154–155 Severe systemic inflammation clinical diagnosis, 64 laboratory studies, 65–66 patient at risk, 64 physical examination, 64–65 severity markers, 66–67 treatment immunologic enhancement, 70–71 inhibition of inflammation mechanisms, 69–70 rapid resuscitation, 67–69 source control, 69 Shock clinical diagnosis Ebb phase, 7–8 flow phase, and decreased oxygen utilization cytopathic hypoxia, 5–6 decreased oxygen delivery, 4–5 historic concepts of, and increased oxygen utilization, management principles, multiple organ dysfunction, Shunt equation, 89 SIMV See Synchronized intermittent mandatory ventilation Sodium reabsorption, 125–126 Spinal cord injury, 182–183 Starling’s equation, 94–95 Starling’s law of heart, 13 Stomach and duodenum 151 Stressed venous return, 16–17 Submassive pulmonary embolism, 111–112 Submassive transfusion, 187 Surgical critical illness hypoadrenalism, 143–144 Surgical nutrition, 161–162 Symmetrical downward brainstem displacement, 178 Symptomatic hypocalcemia, 144–145 Symptomatic hyponatremia, 140 Synchronized intermittent mandatory ventilation (SIMV), 116 Systemic inflammation circulation deficits, 58–60 excess inflammatory toxins, 60 and host-defense deficits, 63 Systolic malfunction, 60 Tachycardia, 17 Tamponade, pericardial, 39–40 TBI See Traumatic brain injury Temporal lobe herniation, 177 Tension pneumothorax, 40 Tertiary peritonitis, 160–161 Thermodilution, 21–22 Thrombocytopenia, 189 Tidal volume (VT), 86 Tissue oxygen measurement, 22–23 Tissue pCO2 measurement, 23 Total body perfusion, 17–19 Total compliance (CT), 91 Total venous capacitance, 16 Trainee, critical care surgeon, 1–2 Transpulmonary pressure (Ptrans), 94 Traumatic brain injury (TBI) adjuncts in management, 180–181 associated organ malfunction acute lung injury, 181 coagulation disorders, 181 diabetes insipidus, 181 hypoadrenalism, 182 myocardial dysfunction, 182 management priorities for patients, 183–184 Triangle of death, 77 Tubular reabsorption, 125 Two-compartment lung model, 112 Type hepatorenal syndrome, 152 Type hepatorenal syndrome, 152 Type I heparin-induced thrombocytopenia, 189 Type II heparin-induced thrombocytopenia, 190–191 Ultrasound, 22 Unstressed venous return, 16–17 Uremia, 132 Urinalysis, 129 Urine electrolytes and creatinine, 129 osmolality, 128–129 specific gravity, 128–129 Variceal hemorrhage, 151 Vascular resistance arterial, 15 factors affecting, 16 Vasodilator therapy, 32 Vasopressor agents, 31 VD See Dead space Venous compliance, 16 Venous lines complications, 28–29 indications for hemodynamic monitoring, 29–30 Venous pressure measurement, 20–21 Venous return description of, 16–17 factors altering, 18 Ventilation, mechanical adjuncts to ventilator management, 119 common ventilator modes, 115–116 flow-pressure waveforms, 113–114 indications, 113 protective ventilator management, 117–118 ventilator-induced lung injury, 117 ventilator strategies, 118–119 Ventilator-induced lung injury (VILI), 117 Ventricular afterload, 12 Ventricular physiology 12–15 VILI See Ventilator-induced lung injury Virchow’s triad, 110 Vital signs, pathological inflammation 64 VT See Tidal volume Water reabsorption, 127 Wittmann patch, 82 Work of breathing, 94 Wound healing, 53–54 ... adequacy of the circulation (where is the hole?), the etiology of an inadequate 20 THE CLINICAL HANDBOOK FOR SURGICAL CRITICAL CARE circulation (why is the hole there?), and the effect of therapeutic... another specialty the acute care surgeon THE ACUTE CARE SURGEON The acute care surgeon combines the interests and expertise of the trauma surgeon, the critical care surgeon, and the general surgeon... to the underlying surgical disease or procedure Thus, the practicing surgeon may have difficulty answering the question “Why is the hole there?” for some patients THE CLINICAL HANDBOOK FOR SURGICAL