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Parental Nutrition

admin — Tue, 07 Jul 2009 05:10:48 +0000

9 PARENTERAL NUTRITION
Margaret M. McQuiggan M.S., R.D., CNSD, Frederick A. Moore M.D.

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.

Posttraumatic Hemorrhagic Shock

admin — Tue, 07 Jul 2009 17:52:17 +0000

17 POSTTRAUMATIC HEMORRHAGIC SHOCK
John B. Moore M.D., Ernest E. Moore M.D.

1. Are hemorrhagic shock and hypovolemic shock the same?

Show answer
Yes.

2. What is hemorrhagic shock?

Show answer
Shock exists when the cardiovascular system is no longer able to meet the body’s metabolic and oxygen needs-inadequate tissue perfusion.
Hemorrhage is the most common cause of shock after injury. Depletion of the vascular volume results in decrease of the driving pressure returning blood to the heart, decrease of the end-diastolic ventricular volume, and decrease in stroke volume; all result in decrease in cardiac output.

3. What is the initial management of hemorrhagic/hypovolemic shock?

Show answer
Prompt and aggressive fluid resuscitation.

4. Describe the cellular manifestations of hemorrhagic shock.

Show answer
Inadequately perfused and oxygenated cells are unable to perform normal aerobic metabolism. This inability results in the production of lactic acid, creating a “gap” metabolic acidosis. The production of adenosine triphosphate (ATP) is decreased, and the cell no longer can maintain membrane polarization/integrity. The first evidence of this is swelling of the endoplasmic reticulum, followed by mitochondrial damage, lysozyme rupture, and the entry of sodium and water into the cell. The loss of interstitial water into cells exacerbates the extracellular and the intravascular volume deficit.

5. List the clinical manifestations of hemorrhagic shock.

Show answer

* Hemodynamic instability with rapid pulse > 100 beats/min and blood pressure < 90 mmHg.
* Altered mental status with lethargy and confusion.
* Decreases in urine output < 0.5 mL/kg/h, central venous pressure, pulmonary capillary wedge pressure, cardiac output, and mixed venous oxygenation saturation (revealed by invasive monitoring).

6. How can blood volume be estimated in adults and children?

Show answer
In adults, multiply the ideal weight in kg × 7% (70 cc/kg).
In children, multiply ideal weight in kg × 9% (90 cc/kg).

7. State the first physiologic response to hypovolemia.

Show answer
The patient tries to compensate for the decrease in stroke volume by increasing heart rate (tachycardia).

8. What are the skin manifestations?

Show answer
The skin becomes cool, clammy, and pale. The subcutaneous veins collapse (making it hard to start an IV line). Capillary refill is delayed ≥ 2-3 seconds.

9. Can the neck veins tell you anything?

Show answer
Lack of pulsations or collapsed external jugular veins indicate low right heart filling pressure (i.e., hypovolemia); conversely, distended veins indicate heart failure or cardiogenic shock.

10. Is the hematocrit a reliable guide for estimating acute blood loss?

Show answer
No. A decrease in the hematocrit occurs with refill of the intravascular space from the interstitial space or during administration of exogenous crystalloid resuscitation fluid. This process is not immediate, and serial hematocrits do reflect blood loss.

11. What is the appropriate choice for IV solution during resuscitation?

Show answer
Lactated Ringer’s or normal saline. Isotonic crystalloid fluid requirements in hemorrhagic shock are estimated at three times the blood loss (3:1 rule). The initial volume replacement should be directed by the response to therapy rather than relying on estimated blood loss (the amount of blood on the pavement is a guess). Don’t add dextrose to the initial fluids; this just exacerbates the physiologic hyperglycemia and provokes an osmotic diuresis. Dextrose 5% is added to IV solutions after initial resuscitation for its protein-sparing effect in the fasting trauma patient.

12. What is base deficit, and how is it useful during resuscitation?

Show answer
Base deficit depends on the hematocrit, pH, and Pco2 and provides information on the metabolic component of acidosis. If you correct the Pco2 back to 40 mmHg, the pH should be 7.40. If your patient is still acidotic, he or she has a base deficit. The worse the base deficit, the lower (less adequate) is your patient’s peripheral perfusion.

13. What are the clinical classifications of shock and the associated clinical manifestations?

Show answer
See Table 17-1. But watch out-these estimates are not nearly as accurate or valuable as determining your patient’s response to therapy/resuscitation.
Table 17-1. CLINICAL CLASSIFICATIONS OF SHOCK

14. What are the other types of shock, and how do they differ from hemorrhagic shock?

Show answer
In addition to hemorrhagic/hypovolemic shock, there are neurogenic, cardiogenic, and septic shock. Neurogenic shock (this is uncommon) is caused by sudden loss of autonomic vascular tone, resulting in vasodilation. The systolic blood pressure is low, the pulse pressure is low, but the skin remains warm. Cardiogenic shock (less common in young gunslingers and frequent in the country club set) results from pump failure secondary to intrinsic heart muscle damage (myocardial infarction) or mechanical compression (cardiac tamponade). Septic shock (more common in surgical intensive care unit patients) is characterized by hypotension and low systemic vascular resistance.

15. When should fluid resuscitation be initiated on the multiply traumatized patient?

Show answer
Immediately! Begin therapy (fluid through big IV lines) while you are doing the primary survey directed at life-threatening injuries. It is inappropriate to wait until the trauma patient fits a precise physiologic classification of shock before starting aggressive volume restoration.
KEY POINTS: CLASSIFICATIONS OF SHOCK

1. Hemorrhagic: most common cause of posttraumatic shock; low filling pressures and cardiac output, low SVO2, high SVR.
2. Neurogenic: uncommon; low SVR with bradycardia; skin remains warm.
3. Cardiogenic: pump failure secondary to intrinsic myocardial damage (infarction) or mechanical compression (tamponade); high filling pressures, low cardiac output, low SVO2.
4. Septic: more common in surgical intensive care unit than in trauma bay; initially high cardiac output, low SVR, high SVO2.

16. What are the potential sources of occult blood loss when trying to figure out a patient’s hemodynamic status?

Show answer
The pleural spaces, abdominal cavity, retroperitoneal/pelvic space (pelvic fractures), major long bone fractures, and at the scene externally (”on the sidewalk”). Femur fractures can hide > 1 L of blood, whereas each rib fracture can account for 150 mL.

17. What is the patient called who becomes unstable after the initial resuscitation, and why is it important to recognize this phenomenon?

Show answer
This guy is a “transient responder.” This indicates ongoing blood loss! Look for it (more aggressive work-up) or transfer to a trauma center.

18. When is blood transfusion indicated during initial resuscitation?

Show answer
If the patient arrives who is not responding to aggressive (”wide open”) crysalloid infusion, the patient should receive uncrossed, O-negative packed red blood cells. Do not wait for type-specific blood if immediate infusion is required-the blood bank is not generally using the same clock (they are not as frightened because they cannot see the patient).

19. How does hemorrhagic shock lead to multiple organ failure (MOF)?

Show answer

Severe hemorrhagic shock begins an inflammatory cascade that cannot be reversed in some patients despite adequate resuscitation. During the Vietnam War, the patients in hemorrhagic shock were treated rapidly, but later died as a result of pulmonary failure or adult respiratory distress syndrome (ARDS). Patients with ARDS can be mechanically ventilated but later die from a combination of liver, cardiac, and bone marrow failure or MOF. MOF is the leading cause of late postinjury mortality in 85% of these deaths. In addition to the cellular derangement in ATP synthesis; shock causes the release of platelet-activating factor, interleukin-8, and arachidonic acid metabolites that activate neutrophils to adhere to endothelial cells and release cytotoxic mediators, which blow big holes in the endovasculature, flooding the interstitial space and causing organ damage. The mesenteric circulation is a hotbed of proinflammatory cytokine synthesis (the gut is the “motor for MOF”). In addition to directly activating neutrophils, the mesenteric circulation appears to release agents (probably phospholipases and other toxic lipids) into the mesenteric lymph that cause neutrophil activation and lung injury.

References
WEB SITES

1. http://www.east.org/tpg/endpoints.pdf
2. http://ww.acssurgery.com/abstracts/acs/acs0603.htm
3. http://www.acssurgery.com/abstracts/ascs/acs0501.htm

BIBLIOGRAPHY
1. American College of Surgeons: Shock. In Advanced Trauma Life Support, 6th ed. Chicago, American College of Surgeons, 1997, p 97.
2. Capone AC, Safar P, Stezoski W, et al: Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock. J Am Coll Surg 180:49, 1995.
3. Choi P, Yip G, Quinonez L, Cook D: Crystalloid versus colloids in fluid resuscitation: A systematic review. Crit Care Med 27:200, 1999. Medline Similar articles
4. Holcroft JW: Shock. In American College of Surgeons: Surgery: Principles and Practice. New York, Web/MD, 2002, p 63.
5. Moore EE: Blood substitutes: The future is now. J Am Coll Surg 196:1, 2003. Medline Similar articles
6. National Institutes of Health Consensus Conference: Perioperative red blood cell transfusion. JAMA 260:270, 1988.
7. Peitzman AB: Management of shock. In Moore EE, Mattox KL, Feliciano DV (eds): Trauma, 5th ed. New York, McGraw-Hill, 2003.

Nutritional Assessment & Enteral Nutrition. Enteral Nutrition

admin — Tue, 07 Jul 2009 04:48:17 +0000

ENTERAL NUTRITION

10. When should enteral nutrition be considered?

Show answer
Always, but especially when a patient is unlikely to meet > 70% of nutritional needs by mouth. Patients who have sustained major head injury (Glasgow Coma Scale score < 8), major torso trauma, major trauma to the pelvis and long bones, or major chest trauma benefit from enteral nutrition. Approximately 85% of postoperative patients (even those undergoing gastrointestinal [GI] surgery) tolerate early enteral feeding (within 24 hours).

11. How do you access the GI tract for feeding?

Show answer
By blind placement of a nasogastric (NG) tube or duodenal placement of a nasoduodenal tube. More distal placement may be achieved endoscopically with a nasojejunal tube (NJ). Gastric decompression and nasojejunal feeds may be accomplished concurrently after endoscopic percutaneous endoscopic gastrostomy or jejunostomy (PEG or PEJ). Alternatively, a gastrostomy or feeding jejunostomy may be placed intraoperatively.

12. What types of enteral formulas are available?

Show answer

Polymeric enteral feedings are soy-based, lactose-free products that contain intact protein, carbohydrates, and fat. Most offer 1 kcal/mL and 37-62 g of protein per liter. Some have additional insoluble or soluble fiber. Special modifications of the standard formulas include “immune-enhancing” agents such as fish oil, arginine, glutamine, and nucleotides. “Elemental” formulas contain amino acids, di-, tri- and quatra-peptides, dextrose, and minimal fat. Several concentrated formulas (2 kcal/mL) are available for use in patients with congestive heart failure (CHF), renal failure, and hepatic failure. In general, products that are disease specific or contain nutrients in elemental form are more expensive than standard products.

13. Are specialized formulas necessary for critically ill patients with diabetes mellitus?

Show answer
No. Formulas with reduced carbohydrates and increased fat loads are marketed as being superior in maintaining glycemic control. These products have not undergone prospective, randomized, controlled trials (PRCTs) to demonstrate superior outcome in ICU patients. The use of standard high-protein formulas in an isocaloric or hypocaloric load combined with appropriate insulin therapy may be the most effective treatment for insulin resistance in stressed type 2 diabetic patients. Glycemic control associated with enhanced outcome is best achieved with insulin, as opposed to carbohydrate restriction. Furthermore, gastric feedings with high-fat formulas in diabetic patients with gastroparesis may be associated with delayed gastric emptying and increased risk of aspiration.

14. Should specialized “pulmonary” formulas be used on all patients on ventilators?

Show answer
No. Specialized high omega-6 fat formulas have been marketed to reduce CO2 production in COPD patients who are CO2 retainers. In theory, these minimize CO2 retention and facilitate weaning. However, avoidance of overfeeding is more beneficial than provision of a high-fat formula.

15. What complications are related to enteral support?

Show answer
Electrolyte abnormalities, hyperglycemia, GI intolerance, pulmonary aspiration, and nasopharyngeal erosions.

16. Should one wait for bowel sounds or flatus before beginning enteral feedings?

Show answer
No.

17. Should one delay nutrition support longer in obese patients, assuming they have increased reserves?

Show answer
No. Obese patients have more fat, but during stress, all patients become hypermetabolic and break down endogenous protein stores to mobilize amino acids for gluconeogenesis, protein production, and energy production. So, even obese individuals “auto-cannabalize.” As with normal-weight patients, obese patients require high-protein nutritional supplementation to meet increased amino acid demands. Theoretically, by providing nutritional support, protein breakdown is minimized.

18. Should enteral formulas be diluted for initial presentation?

Show answer
No. Dilution delays the attainment of feeding goals. Manipulation of the formula increases the likelihood of bacterial contamination. Furthermore, solution osmolarity is a relatively minor culprit in the incidence of diarrhea.

19. How should enteral feeding-related diarrhea be managed?

Show answer
Mild diarrhea usually requires no treatment. Moderate to severe diarrhea may require feeding reduction, antidiarrheal agents, and stool studies for Clostridium difficile. The medication profile should be evaluated for sorbitol-containing elixirs, laxatives, stool softeners, and prokinetic agents. Sanitation issues related to formula handling must be monitored. Some success has been reported with lactobacillus (yogurt) in antibiotic-associated diarrhea or with soluble fiber.

20. Do enteral feedings contain enough water to meet all fluid needs?

Show answer
Most 1-kcal/mL formulas (standard) contain 85% water by volume, and 2-kcal/mL formulas contain 70% water. Water is generally not an issue in ICU patients receiving multiple intravenous (IV) fluids and drugs. However, on the wards or in patients bound for home or postcare facilities, it is essential to write a water prescription with the tube feeding order. General guidelines for the total water needs of patients are shown in Table 8-5.
Thus, if the total calculated need for fluid is 2400 mL for a 60-kg patient and the tube feeding provided 2000 mL of free water, an order should be written to deliver 200 mL of water to the patient twice daily.

Table 8-5. DAILY WATER NEEDS IN RELATION TO AGE

21. How is enteral nutrition infused?

Show answer
Enteral nutrition is generally infused continuously, in bolus form, or cyclically. Continuous infusion is preferred in critically ill patients who require postpyloric feedings. Bolus feedings are generally used in more stable patients with gastric feedings. Cyclic feedings or nocturnal feedings benefit patients who are on concurrent oral intake and in transition to full oral support.

22. Is enteral nutrition better than total parenteral nutrition (TPN)?

Show answer
Yes. Substrates delivered enterally are better tolerated, are associated with fewer metabolic and hepatic complications, and help preserve normal mucosal (”barrier”) integrity. A review of five studies contrasting TPN with no nutrition or early enteral nutrition concluded that TPN is associated with a greater incidence of septic morbidity.

Fluids, Electrolytes, Gatorade & Seat

admin — Mon, 06 Jul 2009 21:19:10 +0000

7 FLUIDS, ELECTROLYTES, GATORADE, AND SWEAT
Alden H. Harken M.D.

1. What is hypertonic saline?

Show answer
Normal saline is 0.9% sodium chloride. Hypertonic saline is 7.5% sodium chloride (eight times as concentrated as normal saline).

KEY POINTS: ION CONCENTRATIONS IN CRYSTALLOID SOLUTIONS

1. ½ NS or 0.45% NaCl: 77 mEq of Na+, 77 mEq of Cl-
2. NS or 0.9% NaCl: 154 mEq of Na+, 154 mEq of Cl-
3. Hypertonic NS or 7.5% NaCl: 1283 mEq of Na+, 1283 mEq of Cl-
4. Lactated Ringer’s: 130 mEq of Na+, 110 mEq of Cl-, 38 mEq of lactate, 4 mEq of K+, and 3 mEq Ca+

2. What is hypertonic saline good for?

Show answer
Resuscitation. The initial hypothesis was that a little hypertonic saline would pull extravascular water into the intravascular compartment, rapidly restoring volume. It now appears that an osmotic jolt (even a transient jump from 140 to 180 mOsm) would pacify circulating neutrophils so that they do not stick to the endovasculature and provoke posttraumatic inflammation.

3. Is hypertonic saline good for anything else?

Show answer
Pacification of “primed” neutrophils should decrease the risk of posttraumatic multiple organ failure.

4. How do you convert 1 g of sodium into milliequivalents (mEq)?

Show answer
Divide by the atomic weight of sodium:

1g (1000 mg) of sodium ÷ 23 = 43.5 mEq

5. How many mEq of sodium are in 1 teaspoon of salt?

Show answer
104 mEq (or 2400 mg).

6. How many mEq of sodium are in an 8-oz bottle of Gatorade?

Show answer
5 mEq.

7. How much does a 40-lb block of salt cost?

Show answer
$3.40 at the feed store.

8. What is the electrolyte content of IV fluids?

Show answer
See Table 7-1.

Table 7-1. ELECTROLYTE CONTENT OF INTRAVENOUS FLUIDS

*Lactate is converted immediately to bicarbonate.

9. How do these concentrations relate to body fluid and electrolyte compartments?

Show answer
See Table 7-2.
Table 7-2. ELECTROLYTE CONCENTRATIONS IN BODY FLUIDS

10. What are the daily volumes (mL/24 h) and electrolyte contents (mEq/L) of body secretions for a 70-kg medical student?

Show answer
See Table 7-3.
Table 7-3. DAILY VOLUMES AND ELECTROLYTE CONTENTS OF BODY SECRETIONS

*See question 6.

11. Are sweat glands responsive to aldosterone? Can they be trained?

Show answer
Yes and yes. Archie Bunker’s sweat contains 100 mEq/L sodium, whereas an Olympic marathon runner retains sodium (sweat sodium may be as low as 25 mEq/L).

12. Is Gatorade really just flavored athlete’s sweat?

Show answer
Yes.

13. What are the daily maintenance fluid and electrolyte requirements for a 70-kg medical student?

14. Does the routine postoperative patient require IV sodium or potassium supplementation? Routine serum electrolyte testing?

Show answer
No and no.

15. Can a patient with a good heart and kidneys overcome all but the most woefully incompetent fluid and electrolyte management?

Show answer
Yes.

16. Can one throw a healthy medical student into congestive heart failure by IV infusion of 100 mL of 5% dextrose in saline solution per kg per hour?

Show answer
No. One will simply be ankle-deep in urine.

17. What is subtraction alkalosis?

Show answer
Vigorous nasogastric suction of a patient with a lot of gastric acid eliminates hydrochloric acid, leaving the patient alkaloti

c.
18. Which electrolyte is most useful in repairing a hypokalemic metabolic alkalosis?

Show answer
Chloride.

19. List the best indicators of a patient’s volume status.

Show answer

* Heart rate
* Blood pressure
* Urine output
* Big-toe temperature

20. Does a warm big toe indicate a hemodynamically stable patient?

Show answer
Most likely. The vascular autoregulatory ability of a young healthy patient is huge. The carotid and coronary circulations are maintained until the bitter end. Conversely, if the patient’s big toe is warm and perfused, the patient is stable.

21. What is the minimal adequate postoperative urine output?

Show answer
0.5 mL/kg/h.

22. What is a typical postoperative urine sodium?

Show answer
< 20 mEq/L.

23. Why?

Show answer
Surgical stress prompts mineralocorticoid (aldosterone) secretion so that the normal kidney retains sodium.

24. Explain paradoxical aciduria.

Show answer
Postoperative patients, by virtue of nasogastric suction (loss of gastric acid), blood transfusions (the citrate in blood is converted to bicarbonate), and hyperventilation (decreased Pco2), are typically alkalotic. Patients also are stressed, and their kidneys retain sodium and water. The renal tubules must exchange some other cations for the retained sodium. The kidney chooses to exchange potassium and hydrogen ions. Even in the face of systemic alkalosis, the postoperative kidney absorbs sodium and excretes hydrogen ions, producing a paradoxical aciduria.
KEY POINTS: MECHANISMS OF PARADOXICAL ACIDURIA

1. Nasogastric suction or refractory vomiting results in loss of gastric acid.
2. Physiologic stress promotes renal retention of sodium and water.
3. To hold on to sodium, the kidney must release other cations (potassium and hydrogen).
4. Counterintuitively, the kidney will release hydrogen ions to keep sodium, resulting in acidic urine.

25. What is third spacing?

Show answer
Hypotension and infection prime neutrophils (CD11 and CD18 receptor complexes), promoting adherence to vascular endothelial cells. Subsequent activation of adherent neutrophils spews out proteases and toxic superoxide radicals, blowing big holes in the vascular lining. Water and plasma albumin leak through the holes. The volume pulled out of the vascular space into the third space of the interstitial and hollow viscus (gut) creates relative hypovolemia and requires additional fluid replacement.

26. What is a Lasix sandwich?

Show answer
25% albumin followed by 20 mg of furosemide (Lasix) IV. If the patient is edematous, the IV albumin theoretically sucks water osmotically out of the interstitial third space. As the excessive water enters the vascular compartment, Lasix produces a healthy diuresis. In most intensive care unit patients, however, the infused albumin rapidly equilibrates across the damaged vascular endothelium. No additional water is pulled into the blood volume. Although surgeons often order Lasix sandwiches, they probably work only in healthy patients who do not need them.

References
BIBLIOGRAPHY
1. Brown MD: Evidence-based emergency medicine: Hypertonic versus isotonic crystalloid for fluid resuscitation in critically ill patients. Ann Emerg Med 40:113-114, 2002. Medline Similar articles Full article
2. Bunn F, Roberts I, Tasker R, Akpa E: Hypertonic versus isotonic crystalloid for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev (1):CD002045, 2002. Full article
3. Greaves I, Porter KM, Revell MP: Fluid resuscitation in pre-hospital trauma care: A consensus view. J R Coll Surg Edinb 47:451-457, 2002. Medline Similar articles
4. Traber DL: Fluid resuscitation after hypovolemia. Crit Care Med 30:1922, 2002. Medline Similar articles

Top 100 Secrets

admin — Thu, 09 Jul 2009 18:49:39 +0000

These secrets are 100 of the top board alerts. They summarize the concepts, principles, and most salient details of surgical practice.

Clinical determinants of brain death are the loss of the
papillary, corneal, oculovestibular, oculocephalic, oropharyngeal, and
respiratory reflexes for > 6 hours. The patient should also undergo
an apnea test, in which the pCO₂ is allowed to rise to at
least 60 mmHg without coexistent hypoxia. The patient should be
observed for the absence of spontaneous breathing.
The estimated risks of HBV, HCV, and HIV transmission by
blood transfusion in the United States are 1 in 205,000 for HBV, 1 in
1,935,000 for HCV, and 1 in 2,135,000 for HIV.
The most common location of an undescended testicle is the
inguinal canal.
The most common solid renal mass in infancy is a congenital
mesoblastic nephroma and in childhood a Wilms’ tumor.
Ogilvie’s syndrome is acute massive dilatation of the cecum
and the ascending and transverse colon without organic obstruction.
The best screening method for prostate cancer is digital
rectal exam combined with serum prostate-specific antigen.
The most common histologic type of bladder cancer is
transitional cell carcinoma.
Carcinoma in situ of the bladder is treated with
immunotherapy with intravesical bacillus Calmette-Guérin.
Localized renal cell carcinoma is treated with surgery
(radical nephrectomy).
The most common cause of male infertility is varicocele.
The most common nonbacterial cause of pneumonia in
transplant patients is cytomegalovirus.
Chimerism is leukocyte sharing between the graft and the
recipient so that the graft becomes a genetic composite of both the
donor and the recipient.
OKT3 is a mouse monoclonal antibody that binds to and
blocks the T-cell CD3 receptor.
The most common disease requiring liver transplant is
hepatitis C.
Cystic hygroma is a congenital malformation with a
predilection for the neck. It is a benign lesion that usually presents
as a soft mass in the lateral neck.
In neuroblastomas, age at presentation is the major
prognostic factor. Children younger than 1 year have an overall
survival rate > 70%, whereas the survival rate for children older
than 1 year is < 35%.
The most feared complication of diaphragmatic hernia is
persistent fetal circulation.
The three most common variants of tracheoesophageal fistula
are (1) proximal esophageal atresia with distal tracheoesophageal
fistula, (2) isolated esophageal atresia, and (3) tracheo-esophageal
fistula with esophageal atresia.
Atresia can occur anywhere in the GI tract: duodenal (50%),
jejunoileal (45%), or colonic (5%). Duodenal atresia arises from
failure of recanalization during the 8th-10th week of gestation;
jejunoileal and colonic atresia are caused by an in utero mesenteric
vascular accident.
The types of aortic dissection are ascending (type A)
dissection, which involves only the ascending or both the ascending and
descending aorta, and descending dissection (type B), which involves
only the descending aorta.
A solitary pulmonary nodule is < 3 cm and is discrete on
chest radiograph. It is usually surrounded by lung parenchyma.
Mediastinal staging is indicated in patients with apparent
or documented lung cancer who have (1) known lung cancer with
mediastinal nodes > 1 cm accessible by cervical mediastinal
exploration, as assessed by CT scan; (2) adenocarcinoma of the lung and
multiple mediastinal lymph nodes < 1 cm; (3) central or large (>

5 cm) lung cancers with mediastinal lymph nodes < 1 cm; and (4) lung
cancer with risk of thoracotomy and lung resection.
The most common causes of aortic stenosis are now
congenital anomalies and calcific (degenerative) disease.
In mitral regurgitation, the left ventricle ejects blood
via two routes: (1) antegrade, through the aortic valve, or (2)
retrograde, through the mitral valve. The amount of each stroke volume
ejected retrograde into the left atrium is the regurgitant fraction. To
compensate for the regurgitant fraction, the left ventricle must
increase its total stroke volume. This ultimately produces volume
overload of the left ventricle and leads to ventricular dysfunction.
The indications for CABG are (1) left main coronary artery
stenosis; (2) three-vessel coronary artery disease (70% stenosis) with
depressed left ventricular (LV) function or two-vessel coronary artery
disease (CAD) with proximal left anterior descending (LAD) involvement;
and (3) angina despite aggressive medical therapy.
Hibernating myocardium is improved by CABG. Myocardial
hibernation refers to the reversible myocardial contractile function
associated with a decrease in coronary flow in the setting of preserved
myocardial viability. Some patients with global systolic dysfunction
exhibit dramatic improvement in myocardial contractility after CABG.
The surgical treatment of ulcerative colitis is total
colectomy with ileoanal pouch anastomosis.
Dieulafoy’s ulcer is a gastric vascular malformation with
an exposed submucosal artery, usually within 2-5 cm of the
gastroesophageal junction. It presents with painless hematemesis, often
massive.
The role of blind subtotal colectomy in the management of
massive lower gastrointestinal bleeding is limited to a small group of
patients in whom a specific bleeding source cannot be identified. The
procedure is associated with a 16% mortality rate.
Colorectal polyps < 2 cm have a 2% risk of containing
cancer, 2 cm polyps have a 10% risk, and polyps > 2 cm have a cancer
risk of 40%. Sixty percent of villous polyps are > 2 cm, and 77% of
tubular polyps are < 1 cm at the time of discovery.
Patients with colorectal cancer with lymph node involvement
(Dukes’ C) should receive chemotherapy postoperatively to treat
micrometastases.
Goodsall’s rule states the location of the internal opening
of an anorectal fistula is based on the position of the external
opening. An external opening posterior to a line drawn transversely
across the perineum originates from an internal opening in the
posterior midline. An external opening, anterior to this line,
originates from the nearest anal crypt in a radial direction.
Incarcerated inguinal hernia: structures in the hernia sac
still have a good blood supply but are stuck in the sac because of
adhesions or a narrow neck of the hernia sac. Strangulated inguinal
hernia: hernia structures have a compromised blood supply because of
anatomic constriction at the neck of the hernia.
Chvostek’s sign is spasm of the facial muscles caused by
tapping the facial nerve trunk. Trousseau’s sign is carpal spasm
elicited by occlusion of the brachial artery for 3 minutes with a blood
pressure cuff.
The two surgical options for Graves’ disease are subtotal
thyroidectomy or near-total thyroidectomy.
The only biochemical test that is routinely needed to
identify patients with unsuspected hyperthyroidism is serum
thyroid-stimulating hormone concentration.
The surgically correctable causes of hypertension are
renovascular hypertension, pheochromocytoma, Cushing’s syndrome,
primary hyperaldosteronism, coarctation of the aorta, and unilateral
renal parenchymal disease.
The “triple negative test” or “diagnostic triad” for
diagnosing a palpable breast mass includes physical examination, breast
imaging, and biopsy.
Chest wall radiation is indicated after mastectomy in
patients with greater than 5 cm primary cancers, positive mastectomy
margins, or more than four positive lymph nodes, all of which are
associated with heightened locoregional recurrence rates.
Sentinel lymph nodes are the first stop for tumor cells
metastasizing through lymphatics from the primary tumor.
The most common site of origin of subungual melanomas is
the great toe. Amputation at or proximal to the metatarsal phalangeal
joint and regional sentinel lymph node biopsy are advised by most
authors.
Ramus marginalis mandibularis, the lowest branch of the
nerve that innervates the depressor muscles of the lower lip, is the
most commonly injured facial nerve branch during parotidectomy.
Waldeyer’s ring is the mucosa of the posterior oropharynx
covering a bed of lymphatic tissue that aggregates to form the
palatine, lingual, pharyngeal, and tubal tonsils. These structures form
a ring around the pharyngeal wall. This may be the site of primary or
metastatic tumor.
A patient in whom the head and neck examination is
completely normal but FNA of a cervical node reveals squamous cancer
should have examination of the mouth, pharynx, larynx, esophagus, and
tracheobronchial tree under anesthesia (triple endoscopy). If nothing
is seen, blind biopsy of the nasopharynx, tonsils, base of tongue, and
pyriform sinuses should be done at the same sitting.
The microorganisms implicated in atherosclerosis include Chlamydia
pneumoniae, Helicobacter pylori, streptococci, and Bacillus
typhosus.
The cumulative 10-year amputation rate for claudication is
10%.
The absolute reduction in risk of stroke is 6% over a
5-year period in asymptomatic patients with > 60% stenosis who
undergo carotid endarterectomy plus aspirin versus patients treated
with aspirin alone (5.1% versus 11%).
Abdominal aortic aneurysm’s average expansion rate is 0.4
cm/year.
Heparin binds to antithrombin III, rendering it more
active.
The patient with suspected intermittent claudication should
initially be evaluated by obtaining ankle brachial index or segmental
limb pressures at rest.
Shock is suboptimal consumption of O₂ and
excretion of CO₂ at the cellular level.
Nitric oxide is synthesized in vascular endothelial cells
by constitutive nitric oxide synthase and inducible NOS, using arginine
as the substrate.
Saliva has the hightest potassium concentration (20 mEq),
followed by gastric secretions (10 mEq), then pancreatic and duodenal
secretions (5 mEq).
Basal caloric expenditure = 25 kcal/kg/day with a
requirement of approximately 1 g protein/kg/day.
6.25 g of protein contains 1 g of nitrogen.
Dextrose has 3.4 kcal/g, protein 4 kcal/g, fat 9 kcal/g
(20% lipid solution delivers 2 kcal/mL).
Maximal glucose infusion rates in parenteral formulas
should not exceed 5 mg/kg/min.
Refeeding syndrome occurs in moderately to severely
malnourished patients (e.g., chronic alcoholism or anorexia nervosa)
who, upon presentation with a large nutrient load, develop clinically
significant decreases in serum phosphorus, potassium, calcium, and
magnesium levels. Hyperglycemia is common secondary to blunted insulin
secretion. ATP production is mitigated, and the classic presentation is
respiratory failure.
Glutamine is the most common amino acid found in muscle and
plasma. Levels decrease after surgery and physiologic stress. Glutamine
serves as a substrate for rapidly replicating cells (interestingly, it
is also the number one metabolic substrate for neoplastic cells),
maintains the integrity and function of the intestinal barrier, and
protects against free radical damage by maintaing GSH levels. Glutamine
is unstable in IV form unless linked as a dipeptide.
Fever is caused by activated macrophages that release
interleukin-1, tumor necrosis factor, and interferon in response to
bacteria and endotoxin. The result is a resetting of the hypothalamic
thermoregulatory center.
Cardiac output = heart rate x stroke volume; normal CO is
5-6 L/min.
SVR = [(MAP - CVP)/CO] x 80; normal SVR is 800-1200
dyne.sec/cm^-5.
Hypovolemic shock: low CVP and PCWP, low CO and SVO₂,
high SVR.
Cardiogenic shock: high CVP and PCWP, low CO and SVO₂,
variable SVR.
Septic shock: low or normal CVP and PCWP, high CO
initially, high SVO₂, low SVR.
Kehr’s sign is concurrent LUQ and left shoulder pain,
indicating diaphragmatic irritation from a ruptured spleen or
subdiaphragmatic abscess. Anatomically, the diaphragm and the back of
the left shoulder enjoy parallel innervation.
Rebound tenderness implies peritoneal inflammation and
irritation not simply abdominal tenderness.
The 5 Ws of post-operative fever are wound
(infection), water (UTI), wind (atelectasis,
pneumonia), walking (thrombophlebitis), and wonder
drugs (drug fevers).
Cricothyroidotomy should not be performed in
patients < 12 years old or any patient with suspected direct
laryngeal trauma or tracheal disruption.
The radial (wrist) pulse estimates SBP > 80 mmHg;
femoral (groin) pulse estimates SBP > 70 mmHg; and carotid (neck)
pulse estimates SBP > 60 mmHg.
A general rule for crystalloid infusion to replace blood
loss is a 3:1 ratio of isotonic crystalloid to blood.
Raccoon eyes (periorbital ecchymosis) and Battle’s sign
(mastoid ecchymosis) are clinical indicators of basilar skull fracture.
CPP = MAP – ICP. Some debate exists on the minimum
allowable CPP, but consensus indicates that a cerebral perfusion
pressure of 50-70 mmHg is necessary.
Violation of the platysma defines a penetrating neck wound.
Tension pneumothorax is air accumulation in the pleural
space eliciting increased intrathoracic pressure and resulting in a
kinking of the SVC and IVC that compromises venous return to heart.
The most common site of thoracic aortic injury in blunt
trauma is just distal to the take-off of the left subclavian artery.
The most common manifestation of blunt myocardial injury is
arrhythmia.
Indications for thoracotomy in a stable patient with
hemothorax include an immediate tube thoracostomy output of > 1500
mL and ongoing bleeding of 250 mL/h for 4 consective hours.
Beck’s triad is hypotension, distended neck veins, and
muffled heart sounds.
The hepatic artery supplies approximately 30% of blood flow
to the liver while the portal vein supplies the remaining 70%. The
oxygen delivery, however, is similar for both at 50%.
The Pringle maneuver is a manual occlusion of the
hepatoduodenal ligament to interrupt blood flow to the liver.
Splenectomy significantly decreases IgM levels.
90% of trauma fatalities due to pelvic fractures are due to
venous bleeding and bone oozing; only 10% of fatal pelvic bleeding from
blunt trauma is arterial (most common site is superior gluteal artery).
Intraperitoneal bladder rupture from blunt trauma:
operative management; extraperitoneal rupture: observant management.
Pseudoaneurysm is a disruption of the arterial wall leading
to a pulsatile hematoma contained by fibrous connective tissue (but not
all three arterial wall layers, which defines a true aneurysm).
The earliest sign of lower extremity compartment syndrome
is neurologic in the distribution of the peroneal nerve with numbness
in the first dorsal webspace and weak dorsiflexion.
Posterior knee dislocations are associated with popliteal
artery injuries and are an indication for angiography.
Management of suspected navicular fracture despite negative
radiography is short-arm cast and repeat x-ray in 2 weeks; at high risk
for avascular necrosis.
Parkland formula: lactated Ringer’s at 4 mL/kg x %TBSA
(second- and third-degree only) of burn. Infuse 50% of volume in first
8 hours and the remaining 50% over the subsequent 16 hours.
The metabolic rate peaks at 2.5 times the basal metabolic
rate in severe burns > 50% TBSA.
Gallstones and alcohol abuse are the two main causes of
acute pancreatitis.
Alcohol abuse accounts for 75% of cases of chronic
pancreatitis.
Isolated gastric varices and hypersplenism indicate splenic
vein thrombosis and are an indication for splenectomy.
The treatment for gallstone pancreatitis is cholecystectomy
and intraoperative cholangiogram during the same hospital stay once the
pancreatitis has subsided.
Proton pump inhibitors irreversibly inhibit the parietal
cell hydrogen ion pump.
Definitive treatment of alkaline reflux gastritis after a
Billroth II includes a Roux-en-Y gastro-jejunostomy from a 40-cm
efferent jejunal limb.
Cushing’s ulcer is a stress ulcer found in critically ill
patients with central nervous system injury. It is typically single and
deep, with a tendency to perforate.
Curling’s ulcer is a stress ulcer found in critically ill
patients with burn injuries.
Marginal ulcer is an ulcer found near the margin of
gastroenteric anastomosis, usually on the small bowel side.
The most common cause of small bowel obstructions is
adhesive disease; the second most common cause is hernias.

Class	Class 1	Class 2	Class 3	Class 4
Description	Blood volume loss = 15% Can compare this with a blood donor	Blood volume loss = 30%	Blood volume loss = 40%	Blood volume loss > 40%
Clinical Manifestations	Occasional mild tachycardia, headache, and postural dizziness	Tachycardia, tachypnea, and decreased pulse pressure	Marked tachycardia, tachypnea, decreased mental status, hypotension, and decreased urine output	Marked tachycardia, marked tachypnea, significantly decreased systolic blood pressure, obtundation to unconscious mental status, and no urine output