• Postoperative fever workup
• opss sepsis 14 days
• solitary pulmonary nodule breast cancer patient
• honeymoon period bochdalek
• relation between breathlessness and total thyroidectomy
• colon surgery diverticulitis
• Hematest-positive NGT
• nonoperative management of spleen injury
• when is the parental nutrion discontinued
• grading for splenic laceration
• having a solitary nodule with calcium flecks
• how many milliequivalents in gatorade

1. What is the physiologic role of the spleen?

Show answer
In fetal development, the spleen serves as a major site for hematopoiesis. In early childhood the spleen produces immunoglobulin M (IgM) and tuftsin. The spleen also functions as a filter, allowing resident macrophages to remove abnormal red blood cells (RBCs), cellular debris, and encapsulated and poorly opsonized bacteria.

2. What injury patterns are associated with splenic trauma?

Show answer
Direct blunt force, deceleration, and compression to the left torso. Think spleen after a motor vehicle accident or fall: lower rib fractures, left side-only rib fractures, and high-energy transfer (big hits) increase the probability of splenic injury.

3. What are the signs and symptoms of splenic injury?

Show answer
The main sign is pain in the left upper quadrant. This is produced by stretching the splenic capsule. Peritoneal irritation (rebound tenderness) is caused by extravasated blood (blood is very irritating). Vital signs vary depending on associated blood loss and are not specific for injuries to the spleen. Unfortunately, a large number of patients with a significant splenic injury exhibit no signs or symptoms at all.

4. What studies can help in diagnosing splenic trauma?

Show answer
Ultrasound (US) can be performed in the emergency department and can rapidly identify as little as 200 mL fluid/blood. When US is not available, diagnostic peritoneal lavage (DPL) is an accurate and sensitive measure of intraabdominal bleeding.
Hemodynamically stable patients permit more thorough evaluations. Although US is extremely sensitive for detecting intraabdominal bleeding, computed tomography (CT) not only can detect and quantify intraabdominal blood but also can characterize specific intraabdominal injuries.

5. How are splenic injuries classified, and why is that important?

Show answer
Management is governed by the hemodynamic status of the patient, but therapy is also influenced by the CT grade of splenic injury. Nonoperative management is most successful in grades I-III, whereas operative intervention is often required for grade IV injuries. Grade V injuries demand prompt operative intervention. (See Table 26-1.)

6. Do splenic injuries require laparotomy?

Show answer
No. Nonoperative management is successful in approximately 95% of patients with grades I-III. Hemodynamically stable patients with evidence of ongoing bleeding (requiring transfusion) may be treated by selective arterial embolization if a bleeding site is identified on angiography.

7. What are contraindications to nonoperative management of splenic injuries?

Show answer

* Hemodynamic instability
* Persistent coagulopathy
* Additional intraabdominal injury requiring operative intervention
. GRADES OF SPLENIC INJURY

8. What is the failure rate of nonoperative management of splenic injury?

Show answer
Any patient with signs of hemodynamic instability, persistent bleeding, worsening pain or tenderness, or progressive injury by CT scanning has failed nonoperative management. Approximately 60% of all splenic injuries can be managed nonoperatively with a failure rate of 12%. Factors that predict nonoperative failure include multiple injuries, grade III-V spleen injuries, age > 55 years, and blood traunsfusion.
KEY POINTS: EXPECTANT MANAGEMENT OF SPLENIC INJURIES

1. Nonoperative management is successful in 95% of grades I-III injuries.
2. 60% of all splenic injuries are managed nonoperatively, with a 12% failure/conversion rate.
3. Factors that predict failure/conversion to operative treatment include injury > grade III, age > 55 years, and blood transfusion requirements.
4. Patients with evidence of ongoing bleeding (e.g., contrast “blush” on CT or ongoing transfusion requirements) may be managed with selective arterial embolization.

9. What is delayed rupture of the spleen?

Show answer
This is a rare complication that occurs in < 1% of patients with a splenic injury. Delayed splenic rupture should be distinguished from a delay in diagnosis of splenic injury and rupture of a known splenic injury. True delayed splenic rupture occurs > 48 hours in a patient with a history of abdominal trauma and no overt clinical evidence of intraabdominal injury on initial presentation.

10. What are the general principles of operative management of the injured spleen?

Show answer
The first priority is to control bleeding. This can usually be accomplished by packing and manual compression of the spleen. If successful, the abdomen is then thoroughly explored for other injuries. Complete mobilization of the spleen by division of the splenocolic, splenorenal, phrenosplenic, and gastrosplenic ligaments is required for complete assessment of the spleen. The short gastric vessels can be ligated with division of the gastrosplenic ligament. Repair of the spleen can be accomplished by application of hemostatic agents, direct pledgeted suture repair of the splenic parenchyma, partial splenectomy, and construction of a “splenic wrap” using absorbable mesh. If splenectomy is required, the splenic artery and vein should be ligated individually prior to removing the spleen.

11. What early complications arise after splenectomy?

Show answer
Bleeding, acute gastric dilatation, gastric perforation, pancreatitis (the splenic artery courses along the top of the pancreas), and subphrenic abscess.

12. What is splenic autotransplantation?

Show answer
Autotransplantation is accomplished by implanting splenic tissue parenchymal slices into pouches created in the gastrocolic omentum.

13. Does splenic autotransplantation preserve splenic function?

Show answer
Autotransplantion after splenectomy is controversial. At least 30% of the original splenic mass is needed to provide normal function. After autotransplantation, IgG and IgM levels are increased in response to pneumococcal vaccine compared with patients after splenectomy alone.

14. Does postsplenectomy leukocytosis predict infection?

Show answer
Elevations in white blood cell (WBC) count and platelet count (PC) after splenectomy are a common physiologic event. After the fourth postoperative day, however, a WBC > 15 x 103 and a PC/WBC < 20 are highly associated with sepsis and should not be confused with the physiologic response to splenectomy.

15. Should a follow-up CT scan be performed after nonoperative management of splenic injuries before patient discharge?

Show answer
No. Most patients who fail nonoperative management do so within 5 days and will exhibit hemodynamic evidence of ongoing hemorrhage. However, follow-up CT should be performed for grade III and IV injuries at 4-6 weeks before getting back to vigorous physical activity.

16. What is OPSS, and how is it prevented?

Show answer
Overwhelming post splenectomy sepsis (OPSS) is a devastating bacteremia (typically encapsulated bacteria) that occurs in 2% of patients after splenectomy. The risk of OPSS is greatest when splenectomy is performed during infancy. The most common organisms are pneumococcus (50%), meningococcus, Escherichia coli, Haemophilus influenzae, staphylococcus, and streptococcus. Although rare, OPSS carries a mortality rate of 75% and has spurred interest in splenic preservation. OPSS is primarily prevented by postoperative vaccination. Pneumococcal, meningococcal, and Haemophilus flu vaccines should be given 2 weeks after splenectomy and are recommended every 5 years. Sepsis can occur despite vaccination; consequently, long-term prophylaxis with oral penicillin is recommended for children.

References
WEB SITES

1. http://www.east.org/tpg/bluntabd.pdf
2. http://www.acssurgery.com/abstracts/acs/acs0506.htm

BIBLIOGRAPHY
1. Cocanour CS, Moore FA, Ware DN, et al: Delayed complications of nonoperative management of blunt adult splenic trauma. Arch Surg 133:619-624, 1998. Medline Similar articles Full article
2. Leemans R, Manson W, Snijder JA, et al: Immune response capacity after human splenic autotransplantation: Restoration of response to individual pneumococcal vaccine subtypes. Ann Surg 229:279-285, 1999. Medline Similar articles Full article
3. Moore EE, Cogbill TH, Jurkovich GJ, et al: Organ injury scaling: Spleen and liver (1994 revision). J Trauma 38:323-324, 1995.
4. Shatz DV: Vaccination practices among North American trauma surgeons in splenectomy for trauma. J Trauma 53:950-956, 2002. Medline Similar articles Full article
5. Toutouzas KG, Velmahos GC, Kaminski A, et al: Leukocytosis after posttraumatic splenectomy: A physiologic event or sign of sepsis? Arch Surg 137:924-928, 2002. Full article
6. Uecker J, Pickett C, Dunn E: The role of follow-up radiographic studies in nonoperative management of spleen trauma. Am Surg 67:22-25, 2001. Medline Similar articles

21. What is the drug of choice for the treatment of an abscess?

Show answer
A knife. Surgically drain the abscess. Abscesses have no circulation of blood within them to deliver an antibiotic. The antibiotic, even if injected directly into the abscess, would be worthless because the abscess contains a soup of dead microorganisms and white blood cells (WBCs). Even if the organisms were barely alive, they would not be reproducing and incorporating the antibiotic. The drug most likely would not work at all at the pH and pKa conditions of the abscess environment.

If there is an indication for an antibiotic, it would be in the circulation around the compressed inflammatory edge of the abscess and the cellulitis (at the vascularized “peel of the orange”) and uncontaminated tissue planes through which the necessary drainage must be carried out. A focal infection is managed by a local treatment, which is both necessary in all abscesses and sufficient treatment in many. Adjunctive systemic antibiotics are occasionally indicated for protection of the tissues through which drainage is carried out. If it helps to make this fundamental surgical principle clear, here is the rule of thumb for management of abscesses: Where there is pus, let there be steel. Perhaps one of the most gratifying procedures in all of medicine is the drainage of pus with immediate relief of local and systemic symptoms (e.g., a perirectal abscess).

22. Which abscess treatment is the important one in determining the outcome of a patient with intraabdominal sepsis?

Show answer
It is the drainage of the last abscess that counts. There should be little applause for drainage of a pelvic abscess in the patient who retains a subphrenic abscess. The patient responds dramatically when the last pus is drained.
This has been an area of significant advance in managing surgical infections because noninvasive scanning capability has facilitated the finding of multiple pockets of pus. Furthermore, such modalities as the computed tomography (CT) scan not only find but also percutaneously direct the fixing of the last abscess. What might have been an indication for an exploratory return trip to the operating room only a decade before (i.e., a failing patient on appropriate therapy should trigger the first response, “Where’s the pus?”) is now a good indication for a CT scan to find and drain the focal infection.

23. Which is preferred for draining an intraabdominal abscess, a needle or a knife?

Show answer
Which can be done most expeditiously? The patient with intraabdominal sepsis is very ill, and the earliest, safe drainage is the procedure of choice. There may be advantages to the less invasive CT scanning, which can be repeated and has less morbidity if the results are negative. Surgery, on the other hand, can fix associated conditions that may have caused the abscess, such as the devitalized loop of bowel or the leak in the anastomosis that can be exteriorized. Each method is likely to find multiple collections, and each can leave external drains for lavage and continuing drainage. Whether by needle or by knife, the urgency and adequacy of local treatment of focal infection determine which methods takes precedence.

24. What is the role of gallium scintiscanning in early finding of abscesses in the abdomen?

Show answer
There is none. Ordering a gallium scan is a temporizing means of self-deception that some progress is being made in finding out what is wrong with the patient. In fact, it merely postpones decisions about intervention in critical illness for several days, often to a point beyond salvage. Gallium scanning involves bowel prepping, a vigorous WBC response from an active bone marrow, and false-positive test results at the sites of tubes and incisions. It is a time-consuming and unreliable test that is the obverse of the principles of early and definitive management. Do not order a gallium scan to satisfy a consultant that “something is being done for this patient.”

23. How fat is fat?

Show answer
Lean body mass is three times more metabolically active than adipose tissue. Multiple definitions of clinical obesity exist: > 120% ideal body weight (IBW), > 130% IBW, body mass index (BMI) > 30, body fat > 24-28% of body weight in men and > 30-35% in women. Measured weight is a poor indicator of relative adiposity. Self-reported weights or weights reported by family members are often erroneous in the ICU setting. Fluid resuscitation and edema make visual assessment challenging and limit the usefulness of noninvasive technology such as bioelectrical impedance (BIA) for measuring body composition. Although measured energy expenditure in kcal/kg of actual weight may sometimes approach that of normal-weight patients, feeding at the measured body weight level may be associated with profound hyperglycemia, hypercapnea, and the inability to clear triglycerides.

24. Should actual, ideal, or adjusted body weight be used in nutrition calculations for obese patients?

Show answer
Studies using an obesity-adjusted weight in kilocalorie calculations (IBW + 0.25 [actual IBW]) report greater correlation with measured energy expenditure than when using actual weight.

25. Which is more important, nitrogen or caloric balance?

Show answer
Ultimately, maintaining a positive nitrogen balance may be more important than achieving a positive kilocaloric balance.

26. Are postpyloric feedings superior to gastric feedings?

Show answer
After major surgery or injury, the stomach exhibits decreased motility for several days. Early enteral feeding, with its known benefits, may not be accomplished through a gastric feeding in the early stages of injury. Jejunostomy feedings have been associated with higher kilocalorie intake, more timely return to anabolism, and a lower pneumonia (aspiration) rate than continuous gastric feeding.

27. When should immune-enhancing formulas be used?

Show answer
Rarely. PRCTs have demonstrated that immune-enhancing diets (IEDs) improve outcome and reduce septic morbidity in patients prone to intraabdominal sepsis after major torso trauma and after major operative resection of upper GI cancers. The use of IEDs should be restricted to these patients, and the duration of use should be limited because of the increased expense. The IEDs have not been adequately tested in other types of patients and, when tested in mixed ICU patients, some evidence suggests that they might even be harmful in addition to being expensive.

28. Are arginine-containing formulas contraindicated in patients with sepsis?

Show answer
Arginine is thought to be a semi-essential amino acid in critically ill patients. It is a metabolic fuel for lymphocytes and fibroblasts. It is also a secretagogue for a variety of hormones (most notably growth hormone). PRTs have shown that supplemental arginine improves wound healing and immune responsiveness in high-risk surgical patients. Arginine is also one of the key ingredients of the newer IEDs. The other key ingredients include glutamine, omega-3 fatty acids, and nucleotides. A large number of PRTs have compared IEDs with standard enteral formula and have shown that IEDs reduce infections and decrease hospital length of stay. The most convincing data come from PRTs that have enrolled patients undergoing major upper GI cancer resections. PRTs that have enrolled less homogenous ICU patients have had a difficult time demonstrating improved outcome, and subset analysis suggest that IEDs may be harmful in ICU patients with sepsis. Reviewing the potential immunomodulating effects of the key ingredients in IEDs has led some authorities to hypothesize that arginine supplementation is harmful in the patients with sepsis. These patients exhibit increased levels of inducible nitric oxide synthase (iNOS). Arginine is a substrate for iNOS and, in its presence, arginine combines the molecular oxygen to produce citrulline and nitric oxide (NO). The resulting NO may have numerous adverse effects in sepsis, including vasodilation, cardiac dysfunction, and direct cytotoxic injury by generating potent reactive oxygen (peroxynitrite) species. Unfortunately, little data support or refute this hypothesis.

29. Should formula with increased fish oil be used in patients at risk for acute respiratory distress syndrome (ARDS)?

Show answer
One industry-funded PRCT demonstrated superior outcome in patients with ARDS when provided a high omega-3 fatty acid enteral product versus a high-omega-6 “pulmonary” formula. Unfortunately, the control diet is not the standard of care and may worsen ARDS. High omega-6 fatty acids increase inflammation and production of lipid mediators, which worsen V/Q mismatch in the lung, which worsen oxygenation in ARDS. Duplication of the results and comparison with standard, moderate-fat polymeric formula is needed.

References
WEB SITE
http://www.gpnotebook.co.uk/simplepage.cfm?ID=516948028

BIBLIOGRAPHY
1. ASPEN Board of Directors and the Clinical Guidelines Task Force: Guidelines for the use of enteral and parenteral nutrition in adult and pediatric patients. J Parent Enter Nutr 26(suppl 1):1SA-138SA, 2002.
2. Cutts ME, Dowdy RP, Ellersieck MR, Edes TE: Predicting energy needs in ventilator dependent critically ill patients: Effect of adjusting weight for edema or adiposity. Am J Clin Nutr 66:1250-1256, 1997.
3. Gadek JE, DeMichele SJ, Karlstad MD, et al: Effect of enteral feeding with eicopentaenoic acid, gamma-linolenic acid, and antioxidants in patients with acute respiratory distress syndrome. Crit Care Med 27:1409-1420, 1999. Medline Full article
4. Konstantinides FN, Konstantinides NN, Li JC, et al: Urinary urea nitrogen: Too sensitive for calculating nitrogen balance studies in surgical clinical nutrition. J Parent Ent Nutr 15:189-193, 1991.
5. Kozar R, McQuiggan M, Moore F: Nutritional support of trauma patients. In Shikora S, Martindale RG, Schwaitzburg S (eds): Nutritional Considerations in the Intensive Care Unit. Silver Spring, MD, Aspen, 2002, pp 229-244.
6. Malone AM: Is a pulmonary formula warranted for patients with pulmonary dysfunction? Nutr Clin Practice 11:189-191, 1997.
7. McClave SA, Snider HL: Understanding the metabolic response to critical illness: Factors that cause patients to deviate from the expected pattern of hypermetabolism. New Horizons 2:139-146, 1994. Medline Similar articles
8. Montecalvo MA, Steger KA, Farber HW, et al: Nutritional outcome and pneumonia in critical care patients randomized to gastric versus jejunal tube feedings. Crit Care Med 20:1377-1387, 1992. Medline Similar articles
9. Moore FA, Feliciano DV, Andrassy R, et al: Enteral feeding reduces post operative septic complications: A meta analysis. Ann Surg 216:62-71, 1992.
10. Talpers SS, Romberger DJ, Pingleton SK: Nutritionally associated increased carbon dioxide production: Excess total kilocalories vs high proportion of carbohydrate kilocalories. Chest 102:551-555. 1992. Medline Similar articles
11. Van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in critically ill patients. N Engl J Med 345:1359-1367, 2001. Medline Similar articles

25. Should all patients undergoing elective laparotomy receive prophylactic antibiotic coverage?

Show answer
No. Doing so would contribute to driving up the cost of antibiotics and their complication rate and devaluing formerly good drugs by rendering them useless against common flora against which they were once highly potent. Operating room nurses have always classified the kind of operation by its status with respect to microbial exposure: clean, contaminated, or septic. These categories are approximation of the microbial risk exposure, and if additionally are superimposed categories of patient resistance (higher risk associated with aging, obesity or other malnutrition, concomitant drugs, or viral or mycobacterial or neoplastic disease immune compromise), these same strata are called class I, II, and III.

26. Which abscess is the most important one to be drained?

Show answer
It is the last abscess that counts in drainage because the patient’s dramatic response is often only achieved when the last pus is drained. Draining a pelvic abscess, for example, but leaving behind a subphrenic abscess, would not result in the quenching of the inflammatory mediators of the sepsis syndrome.
27. Is postoperative fever the earliest and most frequent sign of an incisional infection? Show answer
Postoperative fevers are much more frequent than are wound infections, and the typical wound infection presents far later. The principal sources of postoperative fever are:

* Wind (atelectasis or pneumonia)
* Water (urinary tract infection)
* Walk (get your patient up and around; thrombophlebitis)
* Wound

28. Should you begin amphotericin at the first isolation of Candida species drawn from any intravenous catheter line?

Show answer
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No. Again, remember the distinction between colonization and infection, as well as the source from which the specimen is taken. The IV lines through which hyperalimentation solutions are infused make colonization possible. The presence of a fungus such as Candida species is frequent in patients who do not have an invasive fungal infection or a true candidemia. The latter might be distinguished from catheter colonization by a blood culture drawn from another source, such as a venopuncture. If evidence of any invasive fungal infection is also present (e.g., as endoscopic biopsy of inflammatory mucositis), a choice of antifungal therapies is now indicated.
Topical fungal solutions (e.g., mycostatin mouthwashes or lavage) may control the local fungal infection and may sometimes be instituted as prophylaxis in high-risk patients (e.g., patients on antirejection therapy for bone marrow or solid organ transplantation).
Systemic antifungal agents include fluconazole, caspifungin, and amphotericin.

29. Are antibiotic drug combinations always superior to a single antibiotic agent?

Show answer
Monotherapy is superior to combination antibiotic treatment regimens, but this is provable probably only in the highest-risk patients. With the carbapenem class antibiotic agents, a large multicenter clinical trial proved imipenem therapy superior to aminoglycoside and a macrolide antibiotic, with survival demonstrably superior only in the patients with the highest APACHE scores. Ertapenem monotherapy was the equivalent of ceftriaxone and metronidazole in a smaller, more recent trial.
More is not always better, and the R and S on culture reports does not translate directly to the M and M (morbidity and mortality) at the Death and Complications Conference reports. It is not just important that the effective antibiotic regimen kills the bacteria; also important are how this microbicidal effect is carried out and what effect it may have on the patient in quenching or prolonging the systemic inflammatory response.

30. Is antibody treatment of circulating endotoxin a clinically important tool?

Show answer
Not yet. The neutralization of circulating endotoxin might give a theoretic benefit to patients with sepsis, and animal studies looked promising. But antigen/antibody complexes initiate complement cascade and release of activate leukocyte products such as leukotrienes that may further augment the inflammatory process. The complexes are also filtered in the kidney where they may further impair renal function. To date, no clinical therapeutic benefit has been demonstrated for such monoclonal antibody therapy.

31. What is the role of human recombinant activated protein C in patients with sepsis?

Show answer
Of the multiple clinical trials of mediator neutralization or receptor blockade, the evidence to date seems marginally favorable only for a few, and the major response to treatment comes from early and complete control of the focus of sepsis (not the cytokine sequelae).

References
WEB SITES

1. http://www.acssurgery.com/abstracts/acs/acs0102.htm
2. http://www.medscape.com
* Search: preoperative antibiotics

BIBLIOGRAPHY
1. Bartlett JG: Intra-abdominal sepsis. Med Clin North Am 79:599-617, 1995. Medline Similar articles
2. Bernard GR, Vincent JL, Laterre PF, et al: Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 344:699, 2001.

3. Bilik R, Burnweit C, Shandling B: Is abdominal cavity culture of any value in appendicitis? Am J Surg 175:267-270, 1998.
4. Christou NV, Turgeon P, Wassef R, et al: Management of intra-abdominal infections. The case for intraoperative cultures and comprehensive broad-spectrum antibiotic coverage. The Canadian Intra-abdominal Infection Study Group. Arch Surg 131:1193-1201, 1996. Medline Similar articles
5. Ciftci AO, Tanyei FC, Buyukpamukcu N, Hicsonmea A: Comparative trial of four antibiotic combinations for perforated appendicitis in children. Eur J Surg 163:591-596, 1997. Medline Similar articles
6. Falagas ME, Barefoot L, Griffith J, et al: Risk factors leading to clinical failure in the treatment of intra-abdominal or skin/soft tissue infections. Eur J Clin Microbiol Infect Dis 15:913-921, 1996. Medline Similar articles
7. Geelhoed GW: Preoperative skin preparation: Evaluation of efficacy, timing, convenience, and cost. Infect Surg 85:648-669, 1985.

10. What is an empyema, and what causes it?

Show answer
An empyema is a purulent (infected) effusion. Fluid or blood in the pleural space can be directly innoculated (with bugs) during surgery or trauma (33%) or by contamination from contiguous sites (50%) such as bronchopulmonary infection (most common). Most empyemas are parapneumonic, and the most commonly involved organisms are Staphylococcus aureus, enteric gram-negative bacilli, and anaerobes. Many times, infections are polymicrobial. Often there is no growth of an empyema culture because of effective antibiotic therapy or inadequate culture techniques, particularly with anaerobes.

11. What are the three stages of empyema development?

Show answer
They are the exudative stage (low viscosity fluid), fibrinopurulent stage (transitional phase with heavy fibrinous deposits and turbid fluid), and organizing stage (capillary ingrowth with lung trapping by collagen). This process usually evolves over 6 weeks.

12. How is an empyema diagnosed?

Show answer
Characteristic clinical and radiographic findings are used. Computed tomography (CT) scan is very helpful in defining loculations. Thoracentesis may reveal frank pus, and Gram stain shows many white blood cells (WBCs) and organisms. Biochemical analysis varies, but it is generally an exudate with a low pH (< 7), high LDH (> 1000 IU/L), and low glucose (< 50 mg/dL).

KEY POINTS: THORACIC SURGERY FOR NON-NEOPLASTIC DISEASE

1. Surgery is indicated for complications of tuberculosis, with the most common indication in the United States being multiple drug-resistant tuberculosis with destroyed lung and persistent cavitary disease.
2. An empyema is a purulent (infected) effusion.
3. The three stages of empyema are the exudative stage (low viscosity fluid), fibrinopurulent stage (transitional phase with heavy fibrinous deposits and turbid fluid), and organizing stage (capillary ingrowth with lung trappng by collagen).

13. How should an empyema be treated?

Show answer
Antibiotic therapy directed by Gram stain and culture. If early, tube thoracostomy may be curative. Conversion to open tube drainage (empyema tube) may be necessary if persistent purulent drainage occurs. Instillation of fibrinolytic enzymes (e.g., streptokinase or TPA) may be helpful. An infected loculated (lots of discontinuous cystic pockets) effusion <14 days old should undergo video-assisted thoracoscopic surgery (VATS) decortication (i.e., resection of the thickened, adherent peel). The probability of conversion to open thoracotomy increases with the age of the effusion or empyema.

14. What is a decortication?

Show answer
The cortex is the outside wall or peel of the empyema (like an orange). Thus, decortication is the surgical release and removal of the abscess cavity walls. Successful decortication allows the lung to expand and fill the entire pleural space; if complete expansion does not occur, then the effusion may recur, and continued lung trapping is likely.

15. What are the complications of an empyema left untreated?

Show answer
The most common is pulmonary fibrosis with lung trapping and resultant dyspnea. Others include contraction and deformity of the chest wall, spontaneous drainage through the chest wall (empyema necessitans), bronchopleural fistula, osteomyelitis, pericarditis, mediastinal or subphrenic abscess, sepsis, and death. None of these outcomes is particularly appealing, so in the absence of overwhelming contraindications, all empyemas warrant therapy.

References
WEB SITE
http://www.acssurgery.com
BIBLIOGRAPHY
1. American Thoracic Society: Diagnosis and treatment of disease caused by nontuberculous mycobacteria. Am J Respir Crit Care Med 156(suppl 2 pt 2):S1-S25, 1997.
2. Colice GL, Curtis A, Deslauriers J, et al: Medical and surgical treatment of parapneumonic effusions: An evidence-based guideline. Chest 118:1158-1171, 2000. Medline Similar articles Full article
3. de Hoyos A, Sundaresan S: Thoracic empyema. Surg Clin North Am 82:643-671, 2002. Medline Similar articles

4. Mault JR, Pomerantz M: Mycobacterium tuberculosis and other mycobacteria. Chest Surg Clin North Am 9:227-238, 1999.
5. Pomerantz M, Brown J: Surgery of pulmonary mycobacterial disease. In Kaiser LR, Kron IL, Spray TL (eds): Mastery of Cardiothoracic Surgery. Philadelphia, Lippincott-Raven, 1998, pp 265-271.
6. Wiedeman HP, Rice TW: Lung abscess and empyema. Semin Thorac Cardiovasc Surg 7:119-128, 1995.

1. What does a catheter in the central venous circulation measure?

Show answer
All intrathoracic veins have nearly the same pressure. A catheter in the central venous circulation (anywhere) measures this central venous pressure (CVP) (or right atrial pressure). CVP, plus a little right atrial “kick,” pushes blood into the right ventricle. This right ventricular “filling pressure” is also termed preload.

2. What does a pulmonary artery (PA) catheter measure?

Show answer
A PA catheter (Swan-Ganz catheter) is threaded through the central venous circulation out into the PA. The catheter has three ports-one at the tip and side ports at 4 cm from the tip (the “VIP port”) and 29 cm from the tip (the “CVP port”). With inflation of the balloon at the distal catheter tip and subsequent occlusion of a pulmonary capillary vessel, the transducer at the tip of the catheter “sees” only a static column of blood between it and the left atrium. This pulmonary capillary wedge pressure approximates left atrial pressure or left ventricular filling pressure or LV preload.
When pulmonary vascular resistance is normal, PA diastolic pressure can be used as a substitute for wedge or left atrial pressure. It is not necessary in this circumstance to inflate the balloon to estimate the wedge pressure. This spares the patient the risk of PA rupture from balloon inflation (another advantage is that you do not need to get up to replace the Swan-Ganz catheter when the balloon breaks-usually at 2 a.m.).
A PA catheter can measure blood pressure at three points:

1. The level of the superior vena cava (CVP)
2. The PA (with the balloon deflated)
3. The pulmonary venous pressure/left atrial pressure (with the balloon inflated)

Other important parameters, most importantly cardiac output and mixed venous oxygen saturation, can be measured or calculated based on numbers derived from the PA catheter (see questions 9 and 10).

3. Discuss the complications of central venous catheters and PA catheters.

Show answer
Immediate complications are pneumothorax (2%); inadvertent arterial cannulation (2%); catheter malposition (7%); and, more rarely, air embolism, hemothorax, chylothorax, arrhythmia, brachial plexus injury, vocal cord paralysis, and death (each substantially less frequent than 1%).4 Additionally, “floating” a hard PA catheter across the tricuspid valve and through the right ventricular outflow tract holds the potential for ventricular tachycardia (and if you “nudge” the atrioventricular node, you can provoke complete heart block).
Delayed complications are thrombosis (33% by radiographic studies) and less commonly bacteremia, endocarditis, or clavicular osteomyelitis. Fibrin forms on the catheter within hours of insertion, and the incidence of vessel thrombosis increases with time. PA-related bloodstream infections occur in 4.8 cases per 1000 catheter-days.2 This is roughly equivalent to one bloodstream infection among 100 patients with a catheter in place for 2 days. In autopsy series (clearly not healthy patients), the incidence of infective endocarditis is usually < 2% but increases dramatically with increasing insertion duration.2

4. What are the relative contraindications to percutaneous subclavian or internal jugular venous catheterization?

Show answer
In a patient who is anticoagulated or who has a platelet count < 50,000, it is typically safer to place a central venous line by peripheral cutdown. Inadvertent arterial puncture is tolerated fairly well unless the patient is coagulopathic. A patient with hyperinflated lungs (chronic obstructive pulmonary disease) is more likely to have a pneumothorax during catheter placement.

5. How do you percutaneously place a sheath for PA catheter placement?

Show answer

1. Place the patient in mild head-down (Trendelenburg) position and turn the head toward the contralateral side.
2. Using sterile technique and after administering local anesthesia, insert an 18-G needle on a 10-mL syringe at the point where the deltopectoral groove abuts the clavicle and pointing just north of the suprasternal notch. Hugging the undersurface of the clavicle, apply gentle suction with the syringe. When you hit the vein, dark (nonpulsatile) blood easily flows back into the syringe.
3. Remove the syringe, and insert a soft, flexible wire through the 18-G needle.
4. Remove the needle, leaving the flexible wire in place.
5. Slide a plastic sheath (with the dilator inside) over the guidewire. Remove the wire and the dilator, leaving the sheath in place (if the sheath bleeds profusely, you are in the right place). Aspirate the catheter fully to evacuate all air and flush with saline (Figure 12-1).
6. A chest x-ray must be obtained to confirm proper position and exclude pneumothorax and hemothorax.

Figure 12-1 Catheter placement by percutaneous subclavian vein puncture.

6. As a PA catheter passes through the central venous circulation, what do the pressure waveforms look like?

Show answer
See Figure 12-2.

Figure 12-2 Pressure waveforms after insertion of a Swan-Ganz catheter.

7. What is the value of the CVP and PA pressure?

Show answer
Starling’s law states that (up to a point) increasing end-diastolic volume (preload) increases stroke volume (volume of blood ejected during systole, which is multiplied by heart rate to yield cardiac output). Clinically, we cannot measure end-diastolic volume, so filling pressures are used as a surrogate.
CVP is an estimate of the pressure with which blood flows into the right side of the heart. This number does not reflect left-sided filling pressures. As stated earlier, PA diastolic or wedge pressures allow a better estimate of left-sided filling pressure.

8. Name other parameters that can be measured or calculated with use of a PA catheter.

Show answer
Cardiac output, venous oxygen saturation, pulmonary and systemic vascular resistance.

9. How is cardiac output measured?

There are two ways to use a PA catheter to calculate cardiac output:

1. The technique of thermodilution, in which a volume (10 mL) of saline with known temperature (108°C) is injected into the proximal port of a PA catheter. A temperature probe at the distal catheter tip measures the change in temperature of blood from the time when the cold saline was injected and the time that it passes by the probe. The precise volume and temperature of the injectate allow calculation of the amount of blood passing by the probe, which is a measure of cardiac output. Because cardiac output changes by 15% during the respiratory cycle, injection should be synchronized with end-expiration. A left-to-right intracardiac shunt adds warm blood to the cold saline bolus, giving a falsely elevated measurement of cardiac output.
2. The Fick principle, which relates cardiac output to venous oxygen saturation (see question 11).

10. How is the oxygen content of blood calculated?

Show answer
An oximetric PA catheter has a fiberoptic monitor at its distal tip that continuously measures hemoglobin saturation [So2 (%)]. The catheter tip in the PA measures mixed venous blood (Svo2) oxygenation. After 24 hours of placement, the catheter becomes covered with fibrin, and measurements become less reliable.
The amount of oxygen in blood (Cao2) comprises that portion dissolved in blood (almost nothing) and that portion attached to hemoglobin (lots).
The amount dissolved is calculated by:

O2 dissolved = 0.003 x PaO2

The amount attached to hemoglobin is calculated by:

O2 attached = 1.38 x [Hb] x SaO2

For example, if hemoglobin = 12 g/dL, Pao2 = 60 mmHg, and Sao2 = 90%, then Cao2 = (0.003 × 60) + (1.38 × 12 × 0.90) = 15.08 mL oxygen/100 mL blood. Dissolved oxygen usually comprises only a small percentage of Cao2 (< 1% in this example). Clinically, it is excluded from calculations (see Chapter 6).

11. How is the oxygen content of the blood used?

Show answer
Assuming normal parameters of hemoglobin = 15 g/dL, Sao2 = 96%, and Svo2 = 75%, the difference in oxygen content between the arterial circulation and the venous circulation (A-Vo2) is 4.35 vol%. For every 100 mL of blood that travels around the body, the tissues extract 4.35 mL of oxygen. The normal range for the A-Vo2 is 3-5 vol%.
The Fick principle uses this A-Vo2 to determine cardiac output. Nonstressed patients typically consume oxygen at the rate of 125 mL/min/m2. This is really a “wild guess” because we do not usually determine A-VO2 unless a patient is stressed. By measuring the A-Vo2, we can determine the oxygen contribution for each 100 mL of blood that travels around the body. If the measured A-Vo2 difference = 4.35 mL of oxygen, every 100 mL of cardiac output contributes 4.35 mL to the Vo2 of 250 mL (for a person who is 2 m2, or 2 × 125 mL/min/m2). A total of 5.75 L of blood must travel around the patient’s body each minute to meet the oxygen requirement. By “assuming” Vo2 (typically a big assumption) and by calculating the A-VO2, one can approximate cardiac output.

12. Explain the significance of the Svo2.

Show answer
This is a “poor man’s” cardiac output measure. In a patient with a fixed metabolic rate (or stable oxygen consumption), as cardiac output increases (delivering more blood/min and more oxygen/min), the patient extracts less oxygen per 100 mL of blood peripherally, and more oxygen per 100 mL returns to the right side of the heart (as your patient gets healthier, Svo2 rises). Conversely, as cardiac output decreases (delivering less oxygen/min peripherally to meet fixed demand), the patient extracts more oxygen per 100 mL of blood. Returning venous blood contains less oxygen, and Svo2 decreases. Knowing the the differential diagnosis of a falling Svo2 is important: (1) progressive anemia, (2) cardiac failure, (3) decreasing arterial saturation, and (4) increased basal metabolic rate. The differential diagnosis of a rising Svo2 is (1) sepsis, (2) left-to-right intracardiac shunt, (3) left-to-right peripheral shunt (dialysis access), and (4) inadvertent wedging of the pulmonary artery catheter. The other more gratifying possibility is that your patient is improving in response to your therapy!

KEY POINTS: Svo2 TRENDS

1. “Poor man’s” estimation of cardic output
2. Decreased Svo2: progressive anemia, cardiac failure, decreasing arterial saturation, increased basal metabolic rate
3. Increased Svo2: sepsis, cyanide toxicity, left-to-right intracardiac shunt, left-to-right peripheral shunt, inadvertent wedging of PA catheter

13. How do you determine the systemic (peripheral) vascular resistance (SVR)?

Show answer

SVR = [(MAP - CVP)/CO] x 80
where SVR = systemic vascular resistance (dyne • sec/cm-5), MAP = mean arterial blood pressure (mmHg), CVP = central venous pressure (mmHg), and CO = cardiac output (L/min).
Normal SVR is 800-1200 dyne • sec/cm-5. Multiplying by 80 corrects SVR values from Wood units (mmHg/L/min) to standard metric units (dyne • sec/cm-5).

14. How is a PA catheter used to evaluate shock?

Show answer
Management of the patient in shock requires knowledge of intracardiac “filling” pressures (CVP, PA pressure), cardiac ouput, SVR, and Svo2. Prompt PA catheter placement guides therapy (see Chapter 4 and Table 12-1).
Hypovolemic shock. Right and left filling pressures (CVP and wedge/PA pressures) are low, as are cardiac output and Svo2. SVR is high. The diagnosis is confirmed when volume repletion with rising filling pressure is associated with increased cardiac output, normalization of system pressure, and decreased SVR.
Table 12-1. PA CATHETER EVALUATION OF SHOCK

Cardiogenic shock. Shock despite adequate filling pressures means that the pump is failing. Cardiac output and SvO2 are low. If SVR is high, infuse dobutamine, 5 μg/kg/min, to stimulate the heart and reduce SVR. If SVR is low, infuse epinephrine, 0.05 μg/kg/min, to stimulate the heart and increase SVR.
Septic shock. The hallmarks of septic shock are normal or low-normal filling pressure, supranormal cardiac output, high Svo2, and low SVR (< 600 dyne • sec/cm-5). Treatment requires fluid resuscitation and systemic vasoconstriction while the underlying cause (e.g., abdominal abscess) is treated.

15. What is the evidence supporting the use of a PA catheter?

Show answer
There is no definitive evidence in support of PA catheterization. A prospective trial of > 5700 patients with various disease processes (mostly medical patients) revealed that patients who underwent PA catheterization had higher 30-day mortality, higher hospital costs, and longer intensive care unit length of stay.1
Regardless, we recommend PA catheterization3 for patients with cardiogenic shock, unexplained shock, or unexplained acidosis; all patients undergoing peripheral vascular surgery; and high-risk patients undergoing aortic surgery. Traumatically injured patients, patients with respiratory failure, and critically ill pediatric patients may benefit as well. If you cannot determine what the patient’s volume status is, insert a PA catheter.

16. Do central venous catheters or PA catheters need to be changed on a regular basis?

Show answer
In accordance with Centers for Disease Control guidelines, central venous catheters do not need to be replaced routinely if the exit wounds are dressed properly and sterilized routinely. PA catheters should be changed every 5 days to minimize risks of thrombus and infection.
When catheter-related infection is documented, a new catheter must be placed at a different location. Removed catheters in the setting of bacteremia are always sent for culture.

References
WEB SITES

1. http://www.acssurgery.com/abstracts/acs/acs0606.htm
2. http://www.acpmedicine.com/abstracts/sam/med1401.htm

BIBLIOGRAPHY
1. Connors AF, Speroff T, Dawson NV, et al: The effectiveness of right heart catheterization in the initial care of critically ill patients. JAMA 276:889-897, 1996. Medline Similar articles Full article
2. Mermel LA, Maki DG: Infectious complications of Swan-Ganz pulmonary artery catheters. Am J Respir Crit Care Med 149:1020-1036, 1994. Medline Similar articles
3. Pulmonary Artery Consensus Conference Participants: Pulmonary artery consensus conference: Consensus statement. Crit Care Med 25:910-925, 1997.
4. Ruesch S, Walder B, Tramer MR: Complications of central venous catheters: Internal jugular versus subclavian access: A systematic review. Crit Care Med 30:454-460, 2002. Medline Similar articles Full article

1. What is parenteral nutrition?

Show answer
Parenteral nutrition is the provision of protein as amino acids (4 kcal/g), dextrose (3.4 kcal/g), and fat (lipid 20% solution delivers 2 kcal/mL), vitamins, minerals, trace elements, fluid, and sometimes insulin through an intravenous (IV) infusion. Acid-base status may be influenced by the amount of chloride and acetate used in providing sodium and potassium. The concentrations of calcium and phosphorus are limited to avoid precipitation of a calcium phosphate salt.

2. What are the indications for parenteral nutrition?

Show answer
Parenteral nutrition should be used when the gastrointestinal (GI) tract is totally nonfunctional, such as in major bowel resection, “short gut,” peritonitis, intestinal hemorrhage, paralytic ileus, high-volume enterocutaneous fistulas, ileus, and severe intractable diarrhea (> 1 L/day).

3. What types of access are available for the delivery of parenteral nutrition?

Show answer
Central parenteral solutions are highly concentrated hyperosmolar solutions with osmolarities up to 3000 mOsm/L. These should be delivered into a large lumen vein (e.g., subclavian) or, less commonly, a femoral vein. If a multiple-port catheter is used, a “virgin port” should be reserved exclusively for nutrient infusion. When long-term parenteral nutrition infusion is planned in the postacute setting, a long-term access device (e.g., Hickman or Broviac catheter) may be used. This may not be necessary, however, when the central venous catheter is placed under sterile conditions and the patient or family is taught meticulous care.

4. What is peripheral parenteral nutrition (PPN)?

Show answer
Although used infrequently, PPN may be used when the need for parenteral nutrition is < 7-10 days and central line placement is not desired. Solutions are low osmolarity (< 900 mOsm/L) to prevent thrombosis at the entry site. The inclusion of fat emulsion, which has a near-isotonic osmolarity, helps decrease the overall solution osmolarity while increasing total kilocalories. Because of the dilute nature of the solution, a large volume is required to provide ample nutrition to the patient. Thus, PPN may not be desirable in fluid-restricted individuals, such as patients with congestive heart failure (CHF).

5. Should patients with pancreatitis be exclusively fed parenterally?

Show answer
Although patients with pancreatitis have traditionally been given “gut rest” and total parenteral nutrition (TPN), some studies demonstrate improved outcome with enteral feeding past the ligament of Treitz. The type of formula and level of the GI tract into which nutrients are infused determine the degree to which pancreatic exocrine stimulation is stimulated. TPN is not superior to enteral nutrition in patients with pancreatitis who require nutritional support.

6. Are IV lipids contraindicated in patients with pancreatitis?

Show answer
In instances of pancreatitis caused by congenital hyperlipidemia, lipids should be withheld. This cause is rare in clinical practice.

7. When should concentrated amino acid and dextrose solutions be used?

Show answer
Standard amino acids are generally in an 8.5% (8.5 g/100 mL) or 10% concentration. Concentrated solutions are 15% amino acid. Dextrose is maximally concentrated at 70% solution, although D50% is more commonly used in standard TPN solutions. Maximally concentrated TPN may be desirable in patients with CHF, hepatic failure, or acute renal failure with hemodialysis. Because of increased expense, concentrated amino acids should be used judiciously.

8. Should iron be included in parenteral nutrition?

Show answer
Iron deficiency is rarely an acute intensive care unit (ICU) issue. Blood transfusion delivers 250 mg of elemental iron per unit. In longer-term TPN, iron supplementation may become necessary. Ideally, this should be by the enteral route because of the high anaphylactic potential of IV and intramuscular iron.

9. What complications are associated with parenteral nutrition?

Show answer
Fluid and electrolyte imbalance, altered glucose metabolism, increased liver function tests (LFTs), hepatic steatosis, systemic candidiasis, site infections, and gut atrophy are associated with TPN. Hemothorax or pneumothorax may occur during central line placement. Although rare, air emboli or extravascular placement of central lines have been reported. The reported incidence of catheter-related sepsis (CRS) is variable.

10. What factors play a role in CRS?

Show answer
Preventative measures can be divided into three categories:

1. Catheter insertion
2. Catheter maintenance
3. Catheter removal

During insertion, the skin should be prepared with chlorhexadine rather than alcohol or povidone iodine, and maximal sterile barriers should be used. Although it is commonly thought that multiple lumen catheters have a higher rate of CRS compared with single lumen catheters, randomized studies using rigorous central venous catheter protocols demonstrate comparable rates of CRS. Catheter care should entail scheduled dressing and tubing change every 48-72 hours; antibiotic ointment is of questionable merit (but is commonly used), and gauze is superior to transparent occlusive dressing. Finally, removing the catheter at set intervals effectively reduces CRS, but the benefits must be weighed against the risks of mechanical complications associated with a new catheter placement at a different site. Guidewire changes at set intervals are of debatable value but may be an effective method for early diagnosis of local catheter colonization or infection. Antimicrobial and antiseptic-bonded catheters are now available, and studies indicate that their use reduces the incidence of CRS. These devices cost substantially more than standard catheters and should therefore be limited to usage in high-risk patients.

11. Why do parenterally fed patients often develop hyperglycemia?

Show answer
Parenterally fed patients may develop hyperglycemia because of increased stress and the inflammatory response, limited mobility, concurrent steroid therapy, and excessive kilocalorie intake. Glucose infusion rates should not exceed 5 mg/kg/min.

12. How should hyperglycemia be managed?

Show answer
Information on the home glucose control regimen should be taken from the medication history. Regular insulin may be required in the initial TPN in patients with baseline hyperglycemia, insulin resistance, or insulinopoenia. Supplemental insulin needs should be evaluated daily before reordering TPN. Maintaining the blood glucose < 110 mg/dL has been shown to significantly improve patient outcome. Tight control may merit the usage of continuous IV regular insulin (i.e., insulin drip). NPH insulin is geared toward patients consuming meals at regular intervals and, thus, is not appropriate with continuous IV feedings.
KEY POINTS: HYPERGLYCEMIA SECONDARY TO PARENTERAL NUTRITION

1. Cause: increased stress and inflammatory response, limited mobility, concurrent steroid therapy, overfeeding.
2. Glucose infusion should not exceed 5 mg/kg/min.
3. Supplemental insulin may be required in the parenteral formula.
4. Maintaining blood glucose < 110 mg/dl improves patient outcome.

13. Why are IV fat emulsions used, and when are they contraindicated?

Show answer
Theoretically, fat emulsions are used to prevent essential fatty acid deficiency. In reality, this condition is rare, takes several weeks to develop, and requires only 3-4% of kilocalories as linoleic acid (or 10% of kilocalories as a standard fat emulsion). Fat emulsions are also used to provide additional kilocalories after glucose infusion has reached 5 kcal/kg/min. Practically speaking, lipids are packaged and billed in 100-cc, 250-cc, and 500-cc units; therefore, they are generally included in TPN formulations in these standard volumes. Fat emulsions should be avoided with hyperlipidemia-induced pancreatitis (a small percentage of most pancreatitis) and when serum triglycerides are significantly elevated (e.g., < 500 mg/dL). When delivered in total-nutrient admixtures (three-in-one solutions), lipid emulsions are stable for 24 hours. When infused as a sole nutrient, hang times should not exceed 12 hours because of the potential for bacterial growth.

14. What is refeeding syndrome?

Show answer
Refeeding syndrome occurs when a patient is moderately to severely malnourished and has limited substrate reserves. Patients typically present with chronic alcoholism or anorexia nervosa, after bariatric surgery, or as a result of chronic starvation. When presented with a large nutrient load, the patient rapidly develops clinically significant decreases in serum potassium, phosphorus, calcium, and magnesium levels because of compartment shifts of these elements. Hyperglycemia is commonly caused by blunted basal insulin secretion.

15. How is refeeding syndrome best managed?

Show answer
Ample quantities of potassium, phosphorus, calcium, and magnesium should be provided with the initial parenteral mixtures within the solubility limits of the solution. The initial kilocaloric provision should be reduced by 25% of goal by reducing dextrose kilocalories. Blood glucose is monitored three to four times daily, and serum K, PO4, Ca, and Mg should be evaluated daily for 5 days after initiating feeding while the kilocalories are advanced to goal levels.

16. How should parenteral nutrition be monitored?

Show answer
Parenteral nutrition should be monitored daily with a chemistry profile (Na, K, Cl, CO2, glucose), Mg, phosphorus, and Ca during the first several days of initial therapy in the critical care setting. Accucheck blood glucose determinations are needed every 6 hours. As the fluid and electrolyte balance achieves stability, frequency may be reduced to 1-2 times weekly. The adequacy of the regimen may be assessed by evidence of proper wound healing, maintenance of hydrational status, preservation of body cell mass, and a timely repletion of constitutive protein levels. Overfeeding may be evidenced by insulin resistance, hypertriglyceridemia, increased LFTs, and hypercapnia.

17. What infusion schedules are used for TPN?

Show answer
TPN is most often delivered by continuous infusion. In more ambulatory patients and those on home therapy, a cyclic or nighttime infusion schedule may be adopted as long as adequate hydration can be maintained. This dictates a 12- to 18-hour infusion period.
18. How should TPN be discontinued? Show answer
When TPN is no longer needed, the infusion rate should be reduced by half for 2 hours, halved again for 2 hours, and then discontinued. This “ramp down” prevents reactive hypoglycemia.

19. What is the cost of parenteral nutrition?

Show answer
Parenteral solution costs may vary widely depending on the constituents. The cost of TPN solution components, preparation, access devices, and laboratory monitoring costs approximately 10 times that of a standard enteral feeding. Many third-party payers do not provide more reimbursement for parenteral therapy than enteral in the hospital setting.

1. Have modern antibiotic developments controlled many, if not most, of the problems of surgical infection?

Show answer
No. In seriously ill surgical patients in intensive care unit (ICU) settings, the problems of sepsis have increased and remain among the principal causes of death in ICU patients, especially those with multiple organ failure and impairments of host defense. Antibiotic treatment may change the biographical sketch of the flora associated with patients’ deaths but cannot overcome the multiple causes of failing host resistance to infection that accompany barrier breeches to microbial invasion and the inflammatory and immunologic responses to the “usual suspects.”

2. What kinds of barrier breech allow microbial invasion that may set up surgical infection?

Show answer
The skin and mucosal linings of the body maintain a barrier between the multifloral outside world and the sterile interior milieu of the tissues and organs (even when the outside world is a tube of heavily populated flora through the middle of usually sterile body cavities, such as the gastrointestinal [GI] tract). It is easy to see the barrier breech when a knife penetrates the skin, carrying exterior flora beneath the skin, or when that knife perforates and spills the contaminated contents of the gut into the abdomen. It is less obvious when the breech is caused by a low-flow state or when inadequate nutrition or toxins impair mucosal immunoglobulins, making the “bug-body barrier” permeable. These polymicrobial communities of organisms may begin to invade through the breech in such barriers, particularly if there are further failures in the third line of defense in humoral and cellular resistance.

3. What is the difference between contamination and infection?

Show answer
The presence of microorganisms does not an infection make!
Resident communities of flora on body surfaces do little harm, and gut flora are even beneficial when contained in the gut. It is even possible for bacteria to be transiently present outside their usual commensal residences without constituting an infection in the normally intact host. For example, in vigorously brushing one’s teeth, gram-negative bacteria of various kinds that are resident in the oral cavity are introduced into the bloodstream but probably quickly were eliminated by normal defense mechanisms-unless they met lowered host resistance or seeded a prosthetic heart valve.

4. How can the enormous load of bacteria in the lower GI tract be beneficial?

Show answer
Bugs can be beautiful. These are the same bacteria that have lived with and in humans symbiotically for millennia. They synthesize vitamin K-something we literally cannot do without-or crowd out pathogenic organisms by their overwhelming numbers. They also help to metabolize bile salts and play a role in detoxifying some environmental hazards, similar to septic systems.

5. Whenever intraabdominal bowel spillage is encountered, is it mandatory to culture the fecal contamination and obtain sensitivities of all identified organisms?

Show answer

No. There is a difference between contamination and infection. Therefore, cultures of fecal spillage into the peritoneum will not provide useful information. The contaminant, just because of its change in position with reference to the bowel wall, is not likely to be sterile. When would you like the laboratory to quit? Will you be content to hear a report of Escherichia coli and bacteroides, two of the more than 800 species that even the most compulsive laboratory can hardly be competent to identify, given the exposure to air and time lapse until processing on different media? How will information from a sampling error of mixed, community-acquired contaminants change your therapy? If, for instance, no anaerobes are identified from the fecal specimen, will you be so confident that they are not present as to exclude these species from coverage?
The lesson to be learned is that culture of community-acquired contaminants is expensive, incomplete, and unedifying; the culture of invading microbes in infections, particularly hospital-acquired microbes that persist after treatment, may give critical information and is a more appropriate use of microbiologic resources.

6. What are preps (e.g., bowel preps)?

Show answer
Preps are decontamination procedures, designed to reduce resident flora before an elective invasive procedure. Preps may take the form of a simple process such as an alcohol swab smeared over the skin before a quick prick of the subcutaneous injection or may involve preparation of a larger area of the skin surface for the surgical field of incision (see question 7).
A bowel prep is similarly designed to reduce the resident flora in the gut through (1) mechanical catharsis (i.e., purge); (2) osmotic or volume dilution with large volumes of saline, other electrolyte solutions, or mannitol; or (3) oral administration of nonabsorbed antibiotics. Of these methods, the most important is clearly mechanical catharsis because it purges huge amounts of flora, which may account for up to two thirds the dry weight of colon contents. One of the most cogent reasons for the choice of certain oral antibiotics in bowel preps (see question 9) is their vigorous cathartic action.

7. How is the skin or mucosal cavities of a patient sterilized to prepare a sterile field for operative incision?

Show answer
There is one way, hardly recommended, by which patients can be “sterilized”: similar to instruments and drapes, they can be placed in an autoclave. But short of this absurd example, the skin is never sterile. Decontamination processes are never perfect, particularly in so complex a tissue with crevices and accessory skin structures in which bacteria reside. Resting gloved hands on a “sterile field” does not include the skin or mucosal surfaces.
At best, we simply reduce the flora to the low-level inoculum that can be handled by most intact host defense systems-as in the example of brushing your teeth-but living tissue surfaces are never “sterile.” A method that kills all microbial organisms from such surfaces would also devitalize mammalian cells and render them more susceptible to lower-level microbial inocula.

8. What means can be used to reduce surface resident flora without further injuring the skin or mucosa?

Show answer

* Volume lavage (for mnemonic value only: dilution is the solution to pollution)
* Defatting, which solubilizes the sebaceous oils that may trap flora
* Microbicidal killing with a bacteriostatic agent

To an amazing extent, one cheap, simple fluid that may serve as a diluent, fat solvent, and antimicrobial is alcohol. Alcohol is nearly ideal as prepping solution, with the minor disadvantages that it is dehydrating and minimally flammable. Because it vaporizes and disappears, flora may spread from interstices, outside the field, or even via aerosolized fallout onto the field, thus requiring the addition of extended-duration bacteriostasis to the alcohol prep.
Iodine also kills bacteria but with a greater hazard to sensitive mammalian cells (it oxidizes the cell walls of small plants). A lower initial concentration of iodine and a longer duration of action can be achieved by incorporation of an iodophor, a substance in nearly universal use in preps. The application of moisture- and vapor-permeable “incise drapes” or desiccation-preventing “ring drapes” may further retard repopulation of flora over the prepped (but still not sterile) field.

9. What are “pipe cleaner” antibiotics?

Show answer
Pipe cleaners are orally administered antibiotic regimens that reduce the flora in the GI tract, from which they are not well absorbed. They are an almost ideal component of bowel preps because they are potent cathartic agents and accomplish the vast majority of their “pipe cleaning” by mechanical purgative action. The most popular pipe cleaners include a neomycin or erythromycin base.

10. What is selective gut decontamination? How does it work?

Show answer
It does not work. This method used pipe cleaners in patients at high risk for the development of sepsis from multiple organ failure with the theoretic aim of reducing the risk involved in barrier breech of the GI tract and inoculation with gut flora. Good experimental evidence indicated that this method should reduce the high mortality rate in seriously ill patients at high risk of surgical sepsis. After prolonged clinical trials, however, it failed to demonstrate a benefit in patient survival. The likely reason is that whereas the laboratory studies were done in intact animal models with functioning host defense systems, failures of defense beyond the barrier breech may explain why selective gut decontamination failed to benefit seriously ill patients. Furthermore, resident hospital flora repopulated the purged gut over time, but with virulent forms of microbes selected by their resistance to the broad-spectrum antibiotics. The method still has some use in patients undergoing procedures such as high-dose chemotherapy or bone marrow transplantation and in some patients isolated in “life islands” (e.g., patients with immunodeficiency diseases or burns).

* Not just low blood pressure
* Not just decreased peripheral perfusion
* Not just limited systemic oxygen delivery

Ultimately, shock is decreased tissue respiration. Shock is suboptimal consumption of oxygen and excretion of CO2 at the cellular level.
2. Is shock related to cardiac output? Show answer
Yes. A healthy medical student can redistribute blood flow preferentially to vital organs. After a 3-4-U bleed, your typical young gunslinger can still think: “four dudes jumped me.”
3. Is organ perfusion democratic? Show answer
No. Limited blood flow always is redirected toward the carotid and coronary arteries. Peripheral vasoconstriction steals blood initially from the mesentery, then skeletal muscle, then kidneys and liver.
4. Is this vascular autoregulatory capacity uniform in all patients? Show answer
No. With age and atherosclerosis, patients lose their ability to redistribute limited blood flow. A 20% decrease in cardiac output (or a fall in blood pressure to 90 mmHg) can be life-threatening to a Supreme Court justice, whereas it may be undetectable in a triathlete.
5. For diagnostic and practical therapeutic purposes, can shock be classified? Show answer
Yes.

1. Hypovolemic shock mandates volume resuscitation.
2. Cardiogenic shock mandates cardiac stimulation (pharmacologic and eventually mechanical).
3. Peripheral vascular collapse shock mandates pharmacologic manipulation of the peripheral vascular tone (and direct attention to the cause of the vasodilation-typically sepsis).

6. Is it advisable to treat all shock in the same sequential fashion?

Ultimately, yes. Whether a cigar-chomping banker presents with a big gastrointestinal bleed (hypovolemic shock) or crushing substernal chest pain (cardiogenic shock), the surgeon should take, the following steps in order:

1. Optimize volume status; give volume until further increase in right-sided (central venous pressure [CVP]) and left-sided (pulmonary capillary wedge pressure[PCWP]) preload confers no additional benefit for cardiac output or blood pressure. (This step is Starling’s law-place the patient’s heart at the top of the Starling curve.)
2. If cardiac output, blood pressure, and tissue perfusion remain inadequate despite adequate preload, the patient has a pump (cardiogenic shock) problem. Infuse cardiac inotropic drugs (β-agonist) to the point of toxicity (typically cardiac ectopy)-lots of frightening premature ventricular contractions. For pharmacologically refractory cardiogenic shock, insert an intra-aortic balloon pump (IABP).
3. If the patient exhibits a surprisingly high cardiac output and a paradoxically low blood pressure (such unusual loss of vascular autoregulatory control is associated typically, but not always, with sepsis), infuse a peripheral vasoconstrictor drug (α-agonist).

7. What is the preferred access route for volume infusion? Show answer
Flow depends on catheter length and radius. Volume may be infused at twice the rate through a 5-cm, 14-gauge peripheral catheter as through a 20-cm, 16-gauge central line (see Chapter 2). Assessment of central venous pressure (and left-sided filling pressure) is necessary if the patient fails to respond to initial volume resuscitation.
8. Should one infuse crystalloid, colloid, or blood? Show answer
If the goal is only to improve preload and to repair cardiac output and blood pressure, crystalloid solution should be sufficient. It is controversial whether infused colloid remains in the vascular compartment. If the goal is to augment systemic oxygen delivery, red blood cells bind much more oxygen than plasma (see Chapter 6). Crystalloid should enhance flow, and blood should augment oxygen delivery.
9. When cardiac preload is adequate, which inotropic agents are useful? Show answer
Dobutamine, epinephrine, and norepinephrine are the chocolate, vanilla, and strawberry of the 32 flavors of cardiogenic drugs. These three drugs are all that the surgeon really needs.
10. Is dopamine the same as dobutamine? Show answer
No. Dopamine stimulates renal dopaminergic receptors and may be useful in low doses (2 mg/kg/min) to counteract the renal arteriolar vasoconstriction that accompanies shock. Dopamine has no place as a primary cardiac inotropic agent.
11. Discuss the use of dobutamine, epinephrine, and norepinephrine. Show answer
See Table 4-1.
12. When is an IABP indicated? Show answer
Mechanical circulatory support is indicated when the preload to both ventricles (CVP and PCWP) has been optimized and further cardiac stimulatory drugs are limited by frightening runs of premature ventricular contractions. Do not be afraid to resort to mechanical support.
KEY POINTS: SUMMARY OF ADRENERGIC AGENTS

1. Dobutamine: β1 agonist (cardiac inotrope) with mild-to-moderate β2 effects (peripheral vasodilation).
2. Epinephrine: combined β- and α-adrenergic agent, with the β effects predominating at lower doses and progressive vasoconstriction accompanying increased doses.
3. Norepinephrine: combined β- and α-adrenergic agonist, with the α effects predominating at all doses.

13. What does an IABP do? Show answer
Diastolic augmentation and systolic unloading.

Table 4-1. USE OF DOBUTAMINE, EPINEPHRINE, AND NOREPINEPHRINE

14. What is diastolic augmentation? Show answer
A soft 40-mL balloon is inserted percutaneously through the common femoral artery into the descending thoracic aorta. The balloon is not occlusive (it should not touch the aortic walls). When it is inflated, it displaces 40 mL of blood and is exactly like acutely transfusing 40 mL of blood into the aorta, augmenting each left ventricular stroke volume by 40 mL. Balloon infusion is triggered off the QRS complex from a surface ECG (any lead). The balloon always is inflated during diastole to increase diastolic blood pressure and augment coronary blood flow (CBF). Eighty percent of CBF occurs during diastole.
KEY POINTS: INTRA-AORTIC BALLOON PUMP

1. Indicated for cardiogenic shock refractory to pharmacologic manipulation.
2. Triggered by QRS complex of surface ECG; inflates during diastole (T wave) and deflates on systole (R wave or at dicrotic notch on aortic pressure curve).
3. 80% of coronary blood flow occurs during diastole.
4. Mechanistically results in diastolic augmentation and systolic unloading (afterload reduction).

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15. What is systolic unloading? Show answer
Balloon deflation is an active (not a passive) process. Helium abruptly is sucked out of the balloon, leaving a 40-mL empty space in the aorta. The left ventricle can eject the first 40 mL of its stroke volume into this empty space-at dramatically reduced workload. An intra-aortic balloon increases coronary oxygen delivery (CBF) during diastole, while decreasing cardiac oxygen consumption just presystole.
16. Name the contraindications to IABP. Show answer
Aortic insufficiency: diastolic augmentation distends and injures the left ventricle.
Atrial fibrillation: balloon inflation and deflation cannot be appropriately timed.

References
WEB SITE
http://www.aic.cuhk.edu.hk/web8/IABP.htm
BIBLIOGRAPHY
1. Harken AH: Cardiac dysrhythmias. In Wilmore DW, Cheung L, Harken AH, et al (eds): Scientific American Surgery. New York, Scientific American, 1999.
2. Holcroft JW: Shock. In Wilmore DW, Cheung L, Harken AH, et al (eds): American College of Surgeons Surgery. New York, WebMD Corporation, 2002.