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KIDNEY AND PANCREAS TRANSPLANTATION

admin — Mon, 13 Jul 2009 19:14:54 +0000

CONTROVERSIES

13. Is HLA (human leukocyte) matching still important?

Show answer
It is somewhat important. Historically, HLA matching was an important consideration when matching cadaver kidneys to recipients. With today’s improved immunosuppressive agents, many transplant surgeons believe that HLA matching is no longer critical. Six antigen match kidneys are still shared nationally and do enjoy some improvement in long-term graft survival. Donor organ quality remains the primary determinant in how well the transplanted organ functions. For example, a poorly matched living-donor kidney will still usually outlast a well-matched cadaveric kidney.

14. Does pancreas transplantation halt the progression of diabetic disease?

Show answer
This is still unproven. Logically, we would expect it to. Regression of neuropathy and eye dysfunction has been reported. Recently, long-term recipients have exhibited some regression of microscopic nephropathy.

15. Are islet cell transplants the answer in the future?

Show answer
Probably, although this has been frustratingly slow to achieve. Recent protocols using new immunosuppressive regimens and new islet cell isolation techniques have shown promise, but long-term data are still not widely available. The process requires that isolated islet cells be extracted from a donor pancreas. These cells are then injected into the portal vein, lodge in the liver, and produce insulin. Theoretically, patients achieve the benefit of a pancreas transplant without the surgical risk.

References
WEB SITE
http://www.transplantation-soc.org
BIBLIOGRAPHY
1. Bartlett ST: Laparoscopic donor nephrectomy after seven years. Am J Transpl 2:896-897, 2002. Full article
2. Donovitch G: Handbook of Kidney Transplantation, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
3. Fioretto P, Steffes MW, Sutherland DER, et al: Reversal of lesions of diabetic nephropathy after pancreas transplantation. N Engl J Med 339:69-75, 1998. Medline Similar articles Full article
4. Morris JP: Kidney Transplantation: Principles and Practice, 5th ed. Philadelphia, W.B. Saunders, 2001.

Basic Care Of Hand Injuries

admin — Wed, 08 Jul 2009 07:24:07 +0000

34 BASIC CARE OF HAND INJURIES
Michael J.V. Gordon M.D., Lawrence L. Ketch M.D.

1. What are the goals of hand repair?

Show answer
Functional considerations override cosmesis in the treatment of hand trauma. There are no minor hand injuries. Initial diagnosis and management determine the final result; expert secondary repair cannot overcome primary errors in diagnosis or decision making.

2. What determines the final outcome of a hand injury?

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It is determined by minimal sacrifice of tissue and primary healing accomplished by early wound closure. Minimization of scar tissue by control of edema, prevention of infection, early wound closure, and vigorous physical therapy produce the optimal functional outcome.

3. What factors influence treatment of hand trauma?

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Mechanism, location, and timing of injury; hand dominance; occupation; age; and general health of the patient.

4. How common are occupational hand injuries?

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Hand injuries result in more days lost from work than any other type of occupational injury.

5. What are the essentials of examination of the hand?

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Inspection of position, color, and temperature often reveals the injury. Location suggests possible injury to underlying structures. Motor, sensory, and Doppler ultrasonic examination are confirmatory. All injuries must be radiographed, and surgical exploration provides the definitive diagnosis.

6. How and where should hand injuries be explored?

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Hand wounds should be explored under tourniquet control with adequate analgesia using delicate instruments in a well-lighted surgery suite. Visual magnification is usually mandatory.

7. How is emergency hemostasis of injured hands achieved?

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In the acute setting (outside the operating suite), no tourniquet should be applied, and there should be no blind clamping of any structures. Hemostasis may be achieved by elevation of the extremity and with direct compression of the wound. This approach prevents injury to delicate underlying structures that are tough to see.

8. How are fingertip injuries treated?

Show answer
If < 1 cm of pulp is disrupted, the wound will heal spontaneously with daily cleansing and dressing with nonadherent, moist gauze. Larger defects may require a skin graft, which can often be provided by defatting the amputated piece. Bone exposure necessitates flap coverage if digital length is to be maintained. Digital nerves cannot be repaired distal to the distal interphalangeal (DIP) joint.

9. What is the classification system for fingertip amputations?

Show answer

Classification for fingertip amputations is based on the amount of remaining sensate volar skin. Although the favorably angulated amputation commonly removes some nail and bone, the volar skin is available for easy coverage. This amputation type is “favorable” for treatment by dressings only, allowing wound repair by contraction and epithelialization. The volarly angulated amputation angle is “unfavorable” for conservative management and usually requires a reconstructive procedure. (Image from Ditmars DM Jr: Fingertip and nail bed injuries. In Kasdan ML (ed): Occupational Hand and Upper Extremity Injuries and Disease. Philadelphia, Hanley & Belfus, 1991, with permission.) (See Figure 34-1.)

Figure 34-1 Fingertip amputations.

10. How are nail bed injuries repaired?

Show answer
Repair of the disruption of the germinal matrix must be meticulously approximated under magnification and the nail bed splinted, preferably with the avulsed part. Subungual hematomas should be evacuated by a hot-tipped paperclip or battery-powered electric cautery. Repair of the disruption of the sterile eponychial fold must be maintained for 3 weeks with Xeroform gauze or with the original nail. Often, nail bed disruption cannot be diagnosed without removal of the nail.

11. What is the initial management of flexor tendon?

Show answer
Flexor tendon laceration is not an emergency, and repair should not be undertaken in the emergency department. If a hand surgeon is unavailable, the wound should be copiously irrigated and sutured and prophylactic antibiotics instituted. This injury can wait for definitive repair.

12. What is the proper management of an open fracture?

Show answer
Open fractures should be cultured and then undergo copious lavage with normal saline or Ringer’s lactate. Broad-spectrum antibiotic coverage should be instituted, and the hand should be splinted in the position of function with a bulky dressing.

13. What is the proper treatment for hand infection?

Show answer
The extremity should be immobilized and elevated, and parenteral antibiotics should be given. The patient should be immediately referred for possible surgical drainage.

14. What is the proper management of human bites?

Show answer
After cleansing of the wound, a radiograph should be taken. The wound should be left open-never closed. Antibiotics should be started, and the wound should be rechecked at 24 and 48 hours. If evidence of infection is present, parenteral antibiotics should be instituted and referred for possible surgical drainage. The so-called fight bite occurs over the metacarpophalangeal (MCP) joint or proximal interphalangeal joint when a clenched fist is impaled on the front teeth of an adversary. This often inoculates the MCP joint with anaerobic streptococci. When infection is diagnosed, immediate arthrotomy and lavage should be performed.

15. How are injection injuries treated?

Show answer
Despite their innocuous appearance, injection injuries may cause profound destruction of hand structures. Any such injury requires immediate hospitalization with prompt and extensive decompression, drainage, and debridement.

KEY POINTS: CARPAL TUNNEL SYNDROME

1. Symptoms: numbness, tingling, pruritus of the palm, thumb, middle, and index fingers.
2. Mechanical cause is compression of median nerve and carpal tendons.
3. Women are affected twice as often as men; the syndrome is more common after 40 years of age.
4. Predilection for people who perform repetitive manual labor.

16. What is carpal tunnel syndrome (CTS)?

Show answer
CTS is the most common peripheral compression neuropathy; it is signaled by numbness and tingling of the hand.

17. Is CTS more common in older or younger people? Men or women?

Show answer
CTS is more common in people older than age 40 years, but an increasing number of young people with CTS have been reported in recent years, usually those whose jobs involve repetitive manual labor. Women are affected approximately twice as often as men.

18. What are the most preventable causes of deformity in hand injuries?

Show answer
Edema and infection lead to increased scarring and restricted function. Prolonged immobilization in a poor position also impairs function, as does delayed skin closure. Failure to obtain a radiograph leads to a missed diagnosis with delay in recognition of an injury.

19. What is the proper emergency department treatment of all hand injuries?

Show answer
The patient should be sedated and the wound cultured and irrigated. A thorough examination must be performed and a sterile compression dressing placed. The upper extremity should be splinted, tetanus prophylaxis should be administered, and broad-spectrum antibiotic coverage should be instituted for crush avulsion or heavily contaminated wounds. Radiographs of the hand should always be obtained.

20. What are the guidelines for replantation of an amputated finger?

Show answer
There are no absolute guidelines. A microsurgeon who is a member of a replantation team should be consulted. If replantation is planned, parts should not be immersed directly in water or put directly on ice or dry ice. The part should be copiously irrigated, wrapped in a moist sponge, and placed in a sterile plastic container; the plastic container should be placed in an ice-water slurry for transport.

References
WEB SITE

* http://www.ninds.nih.gov
o Search: carpal tunnel

BIBLIOGRAPHY
1. Dunn R, Watson S: Suturing versus conservative management of hand lacerations. Hand lacerations should be explored before conservative treatment. Comment on Br Med J 325(7359):299, 2002. Br Med J 325(7372):1113, 2002.

2. Hansen TB, Carstensen O: Hand injuries in agricultural accidents. J Hand Surg 24B:190-192, 1999.
3. Irvine AJ: Suturing versus conservative management of hand lacerations. Incisions are not lacerations. Comment on Br Med J 325(7359):299, 2002. Br Med J 325(7372):1113, 2002; author reply 325(7372):1113, 2002.
4. Lee SJ, Montgomery K: Athletic hand injuries. Orthop Clin North Am 33:547-554, 2002. Medline Similar articles Full article
5. McAuliffe JA: Hand care in the new millennium: Surgeons’ perspective. J Hand Ther 12:178-181, 1999. Medline Similar articles
6. Riaz M, Hill C, Khan K, Small JO: Long-term outcome of early active mobilization following flexor tendon repair in zone 2. J Hand Surg 24B:157-160, 1999.
7. Taras JS, Lamb MJ: Treatment of flexor tendon injuries: Surgeons’ perspective. J Hand Ther 12:141-148, 1999. Medline Similar articles
8. Van der Molen AB, Matloub HS, Dzwierzynski W, Sanger JR: The hand injury severity scoring system and workers’ compensation cases in Wisconsin, USA. J Hand Surg 24B:184-186, 1999.

Queries 3

admin — Fri, 14 Aug 2009 18:10:27 +0000

Queries 5

admin — Mon, 21 Sep 2009 06:21:43 +0000

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

What Is Pulmonary Insufficiency?

admin — Mon, 06 Jul 2009 19:57:22 +0000

5 WHAT IS PULMONARY INSUFFICIENCY?
Alden H. Harken M.D.

1. What is pulmonary insufficiency?

how answer
The alveolar-capillary surface of the lung is the size of a singles tennis court. The purpose of the lung is to match alveolar ventilation (Va) to blood flow (Q). Mismatching leads to pulmonary insufficiency.

2. How is Va/Q mismatching characterized?

Show answer
Shunt: decreased ventilation relative to regional blood flow; pulmonary arterial (unoxygenated) blood “shunts” by hypoventilated alveoli
Dead space: decreased pulmonary regional blood flow relative to ventilation

3. How much energy is expended in the work of breathing?

Show answer
A healthy medical student expends about 3% of total oxygen consumption (energy use) on work of breathing. After injury, particularly a big burn, patients may increase fractional energy expenditure of breathing to 20% of their total energy use.

4. Which surgical incisions most significantly compromise a patient’s vital capacity?

Show answer
Intuitively an extremity incision or injury influences vital capacity least, followed sequentially by a lower abdominal incision, median sternotomy, thoracotomy, and upper abdominal incision. An upper abdominal incision is worse than a thoracotomy!

5. Is a chest radiograph helpful in assessing respiratory failure?

Show answer
Yes but the radiograph must be interpreted carefully. It can be difficult to standardize x-ray technique, especially in an intensive care unit.

6. What should you look for on the chest radiograph of a patient with impending respiratory failure?

Show answer

1. Are both lungs fully expanded?
2. Are there localized areas of infiltrate, atelectasis, or consolidation?
3. Are there generalized areas of infiltrate, atelectasis, or consolidation?
4. Are the endotracheal and other tubes in proper position?

7. Why is the local versus generalized distinction important in assessing respiratory failure?

Show answer
A local process may be produced by tumor or aspiration, and both are diagnosed and treated by bronchoscopy. Generalized multilobar infiltrates are more likely to represent a diffuse alveolar-capillary leak syndrome, such as adult respiratory distress syndrome (ARDS).

8. What is ARDS?

Show answer
A diffuse, multilobar capillary transudation of fluid into the pulmonary interstitium that dissociates the normal concordance of ventilation (Va) with lung perfusion (Q).

9. What governs fluid flux across pulmonary capillaries into the interstitium of the lung?

Show answer
Starling initially described the balance between intravascular hydrostatic pressure (Pc), which tends to push fluid out of the capillaries, and colloid oncotic pressure (COP), which sucks fluid back in across the capillary endothelial barrier (K):

Fluid flux = 5 K(Pc – COP)

10. What causes ARDS?

Show answer
Anything that increases lung dysfunction by promoting wet lung:

1. Heart failure backs up pulmonary intravascular Pc, forcing fluid into the pulmonary interstitium.
2. Malnutrition and liver failure decrease plasma protein and COP. Fluid is not sucked back out of the lung (if the total protein and albumin are low).
3. Sepsis may break down the capillary endothelial barrier (K), permitting water and protein to leak into the lung.

KEY POINTS: CLINICAL FEATURES OF ARDS

1. Severe hypoxemia refractory to increased inspired oxygen concentration
2. Diffuse pulmonary infiltrates
3. Low lung compliance
4. Large V/Q mismatch

11. Explain high-pressure versus low-pressure ARDS.

Show answer
Purists appropriately note that lung congestion resulting from high intravascular hydrostatic pressure secondary to heart failure is really not primary respiratory distress syndrome. If the pulmonary capillary wedge pressure (PCWP) is > 18 mmHg, the diagnosis is high-pressure pulmonary edema (not ARDS). A patient with pure mitral stenosis may have (high-pressure) lung congestion, whereas a malnourished patient may develop (low-pressure) lung congestion; neither of these is, strictly speaking, ARDS, although patients with ARDS frequently have components of both.

12. What is a normal COP?

Show answer
22 mmHg.

13. How is COP calculated?

Show answer
Of COP, 75% normally is created by serum albumin along with globulins and fibrinogen:

COP = 2.1 (total protein)

If an osmotically active molecule such as hetastarch is infused, this calculation is fouled up.

14. Define low-pressure ARDS.

Show answer
Low-pressure ARDS is a redundant term. To make the diagnosis of ARDS, the PCWP must be <18 mmHg. Pure ARDS exists only if the PCWP is > 4 mmHg less than the COP.

15. How can the pulmonary capillaries leak if the COP exceeds the PCWP?

Show answer
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The current concept involves a septic expression of neutrophil CD11 and CD18 adhesion receptors, which stick to pulmonary vascular endothelial intercellular adhesion molecules. Septic stimuli provoke the adherent neutrophils to release intravascular proteases and oxygen radicals. Resultant endovascular damage breaks down the capillary endothelial barrier, permitting the lung leak-even at low hydrostatic pressure.

16. What is a Lasix sandwich?

Show answer
Many surgeons, when their backs are against the wall, give 25 g of albumin followed in 20 minutes by 20 mg of furosemide (Lasix) IV. They reason that the albumin pulls fluid out of the water-logged lung and the Lasix promotes diuresis to rid the patient of extra water. This therapeutic concept probably works only in patients who are not very sick. The sicker the patient, the faster the infused albumin leaks and equilibrates across the damaged endovascular endothelial barrier. Little water is sucked out of the sick lung in preparation for diuresis.

17. List the goals of therapy for ARDS.

Show answer

1. Reduce lung edema (typically with a diuretic).
2. Reduce oxygen toxicity (inspired oxygen concentration < 60% is safe).
3. Limit lung barotrauma (avoid peak inspiratory pressure in > 40 cm H2O).
4. Promote matching of Va and Q; frequently positive end-expiratory pressure (PEEP) is useful.
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output).

18. What governs the distribution of lung perfusion (Q)?

Show answer
Mostly gravity. The dependent portions of the lung always are better perfused.

19. Discuss hypoxic pulmonary vasoconstriction (HPV).

Show answer
Most students believe that after dedicating the entire second year of medical school to pheochromocytoma and HPV, both entities may be safely forgotten. At least in the case of HPV, this is not true. A patient who has just undergone carotid endarterectomy illustrates the relevance of HPV. As the patient awakens from anesthesia, the blood pressure is 220/120 mmHg and arterial PO2 with 100% oxygen is 500 mmHg. So that the patient will not blow the carotid anastomosis, the surgeon urgently infuses nitroprusside. In 20 minutes, the blood pressure is 120/80 mmHg, but PO2 (still with 100% oxygen) has dropped to 125 mmHg!
Did the lab technician screw up the blood gas analysis? No-this is an example of the clinical significance of HPV, which directs pulmonary arteriolar delivery of deoxygenated blood toward ventilated alveoli and away from poorly ventilated lung regions. The patient was using HPV to attain a PO2 of 500 mmHg. All antihypertensive agents (e.g., nitroprusside) and most general anesthetics block HPV. The PO2 increment from 125 to 500 mmHg is due to HPV. HPV steered perfusion toward ventilated areas of the lung.
20. What governs the distribution of ventilation in lung? Show answer
KEY POINTS: THERAPEUTIC GOALS IN ARDS

1. Reduce lung edema
2. Reduce oxygen toxicity (FiO2 < 60%)
3. Minimize barotraumas (keep peak inspiratory pressure < 40 cm H2O)
4. PEEP to promote V/Q matching
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output)

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A large pleural pressure gradient (more negative at the top of the lung by 20 cm H2O) squeezes gas primarily out of the dependent lung during each exhaled breath. The regional compliance of dependent lung is much better than that of lung apex, which still is distended with gas at the end of exhalation. The usual approach is to perfuse and ventilate dependent lung preferentially.

21. How does ARDS compromise lung function?

Show answer
The trachea is held open with cartilaginous rings, but terminal bronchioles are not. Wet lung collapses the terminal bronchioles, trapping distal alveolar gas. Persistent perfusion of these poorly ventilated regions is a shunt that results in hypoxia.

22. How long does it take for pulmonary arterial (deoxygenated) blood to equilibrate completely with trapped (poorly oxygenated) alveolar gas?

Show answer
About three fourths of a second. After that, no more oxygen is added, and no more CO2 is eliminated from the perfusing blood. Terminal bronchiolar closure producing trapped alveolar gas is bad.

23. What is the therapy for terminal airways closure and resultant shunt secondary to the wet lung of ARDS?

Show answer
PEEP should hold open terminal bronchioles, promoting ventilation of previously trapped alveoli and minimizing the shunt.

24. When may the patient come off mechanical ventilation and be extubated safely?

Show answer
The patient should be sufficiently alert to protect his or her airway, require an inspired oxygen concentration no greater than FiO2 = 0.4, and be comfortable breathing on a T-piece (without mechanical ventilation) for 60 minutes at a respiratory rate < 20 and a minute ventilation < 10 L/min. The patient should be able to generate a negative inspiratory force > -20 cm H2O. Finally, after 1 hour on the T-piece, oxygenation should provide a hemoglobin saturation > 85% without respiratory acidosis (see Chapter 6).

25. What is nitric oxide (NO)?

Show answer
NO is synthesized in vascular endothelial cells by constitutive nitric oxide synthase (cNOS) and inducible NOS (iNOS). Intuitively, inhaled NO should diffuse across ventilated alveoli to increase regional perfusion and improve matching of Va/Q.

26. Does inhaled NO work in ARDS?

Show answer
Almost 24 randomized controlled clinical trials have assessed the therapeutic efficacy of inhaled NO. Although systemic oxygenation and pulmonary hypertension improve transiently, ventilator time and ultimate survival are not influenced. Just say NO.

References
WEB SITES

1. http://www.ardsnet.org
2. http://www.nlm.nih.gov/medlineplus/ency/article/000103.htm

BIBLIOGRAPHY
1. Bartlett R: Pulmonary Insufficiency. New York, American College of Surgeons, Surgery WebMd Corporation, 2002.
2. Davidson TA, Caldwell ES, Curtis JR, et al: Reduced quality of life in survivors of acute respiratory distress syndrome compared with critically ill control patients. JAMA 281:354-360, 1999.
3. Gust R, McCarthy TJ, Kozlowski J, et al: Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration. Am J Respir Crit Care Med 159:563-570, 1999.
4. Pesenti A, Fumagalli R: PEEP: Blood gas cosmetics or a therapy for ARDS? Crit Care Med 27:253-254, 1999.

Nutritional Assessment & Enteral Nutrition. Nutritional Assessment

admin — Mon, 06 Jul 2009 21:33:48 +0000

8 NUTRITIONAL ASSESSMENT AND ENTERAL NUTRITION
Margaret M. McQuiggan M.S., R.D., CNSD, Frederick A. Moore M.D.

NUTRITIONAL ASSESSMENT

1. What does a nutritional assessment include? Show answer

1. The medical and surgical history is used to establish preexisting (comorbid) conditions, metabolic stress, and alterations in organ function.
2. The physical examination focuses on the muscle mass, adipose stores, skin integrity, and hydrational state.
3. Laboratory data include the chemistry profile (Na, K, CO2, Cl, BUN, creatinine, glucose), ionized Ca, serum PO4, and Mg, complete blood count (CBC) with differential, arterial blood gases (ABGs; to assess acid-base status and CO2 retention), albumin, transferrin, prealbumin, and urinary nitrogen.
4. The drug profile can reveal agents that affect the metabolism of nutrients (insulin, levothyroxine, corticosteroids) or alter energy expenditure (beta-blockers, Diprivan).
5. Anthropometric data include height and weight; skinfold testing with calipers is only useful once edema has resolved but is rarely used in the acute care setting. Although information on adipose reserve, body cell mass, intra- and extracellular water, and third space fluid may be elucidated, standards for bioelectrical impedance analysis (BIA) have yet to be determined.
6. A nutrition history reveals preexisting nutritional practices.
7. The social history explores economic data or substance abuse behaviors and may predict the likelihood of adequate home care for the patient upon discharge.

2. What are primary and secondary malnutrition?

Show answer
Primary malnutrition is the consumption of inadequate kilocalories, protein, vitamins, or minerals. It may occur because of poor food choices, anorexia, poverty, alcoholism, suboptimal support regimens, or after bariatric surgery. Secondary malnutrition may occur even when adequate food is infused or consumed. It results from organ dysfunction (hypoalbuminemia with cirrhosis), malabsorption (Crohn’s disease), immobility (muscle wasting), drug therapy (insulin resistance with corticosteroids), or the inflammatory response (reprioritization of hepatic synthesis of acute phase instead of constitutive proteins).

3. What is the significance of serum proteins in nutritional assessment?

Show answer

Table 8-1. SERUM PROTEINS

TIBC = total iron-binding capacity.

KEY POINTS: HALF-LIVES OF SERUM PROTEINS USED AS NUTRITIONAL MARKERS

1. Pre-albumin: 2-4 days
2. Transferrin: 8-10 days
3. Albumin: 20-21 days

The most readily available proteins for nutritional assessment are albumin, transferrin, and prealbumin, which are all constitutively produced in the liver. Their half-lives are 20-21 days, 10-12 days, and 2-4 days, respectively. The level of all three plummets shortly after injury or surgery as the liver reprioritizes the production of acute phase proteins. Then, as inflammation, infection, and stress begin to resolve, the liver resumes production of constitutive proteins. Adequate kilocalories and protein facilitate this process. Because of their shorter half-lives, prealbumin and transferrin are most useful in the intensive care unit (ICU) setting and should be limited to patients with creatinine clearance > 50 mL/min. Levels of both proteins may be depleted in patients with hepatic failure or cirrhosis because of decreased synthetic function. Prealbumin travels in the circulation bound to retinol-binding protein (RBP) and vitamin A. Levels of prealbumin may be elevated in renal failure despite nutritional compromise, because of decreased catabolism and decreased excretion of RBP. Transferrin is elevated with iron depletion, independent of the effects of nutrition. (See Table 8-1.)

4. What is the significance of urinary nitrogen in nutritional assessment?

Show answer
Total urinary nitrogen (TUN) is the most reliable indicator of nitrogen utilization and excretion in surgical ICU patients. However, urinary urea nitrogen (UUN) is more readily available in most hospital laboratories. Although TUN and UUN are nearly equal in healthy ambulatory patients, critically ill patients exhibit a poor correlation between the two. Optimal nutrition support should place a patient in 13 to 15 nitrogen balance. One may estimate the protein needs of the patient by adding:

[24 h UUN (g) + 2 g N insensible losses + 3] x 6.25 = required amount of protein (g)

The total in brackets is multiplied by 6.25 to convert nitrogen grams to protein grams. Thus, if the laboratory reported a 13-g UUN/24 hours and a 2-g N insensible loss (skin, hair, feces) + 3 g for optimal anabolism, the patient would require 18 g N × 6.25 = 112.5 g of protein for anabolism. Urinary nitrogen is not useful as a guide for nutritional prescription in hepatic failure, renal dysfunction (< 50 mL/min creatinine clearance), or recent spinal cord injury.

5. How are protein requirements determined?

Show answer
Protein need is determined based on the weight of the patient, current stress factors, extraordinary skin losses, and organ function. Although the recommended daily allowance (RDA) for protein for healthy individuals is only 0.8 g protein/kg body weight, the following guidelines may be used in surgical patients. (See Table 8-2.)
Table 8-2. PROTEIN REQUIREMENTS IN RELATION TO INJURY LEVEL

Injury Level Protein Requirement
Mild stress or injury 1.2-1.4 g/kg
Moderate stress or injury 1.5-1.7 g/kg
Severe stress or injury 1.8-2.5 g/kg

6. Should protein be severely restricted in surgical patients with hepatic failure or renal failure?

Show answer
Protein should be restricted to 0.7 g/kg in patients with encephalopathy, only if the hepatic encephalopathy produces significant clinical consequences. Only 10% of chronic liver disease patients are protein sensitive; thus, other causes of encephalopathy such as infection, constipation, and electrolyte disturbance should be explored. Otherwise, a more typical postsurgical protein load may be adopted (1.4 g/kg). In injured patients with renal failure, one must balance the need for increased protein with the need for increased dialysis. One should provide the amount of protein required and dialyze more frequently.
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7. How are kilocalorie needs determined?

Show answer
There are several methods for setting kilocalorie targets in the surgical patient: standard prediction equations, kilocalorie per kilogram estimations, and indirect calorimetry. One common prediction equation, the Harris Benedict (HBE), was developed in 1919 for use on ambulatory, fasted, healthy people. Basal energy expenditure (BEE), the number of kilocalories required at rest daily, is calculated using the following equations:

Female BEE = 655 + 9.6 (kg) + 1.8 (cm) -4.7 (age)
Male BEE = 67 + 14 (kg) + 5 (cm) – 6.7 (age)

Subsequently, the above sums are multiplied by stress factors to determine total kilocalorie goals. (See Table 8-3).
Many clinicians use a total kcal/kg goal as shown in Table 8-4.
Table 8-3. KCAL NEEDS IN RELATION TO STRESS LEVELS

Stress Level Example Kcal Needs
Mild Closed fracture, pneumonia, or splenic laceration BEE × 1.2
Moderate Bowel resection, hepatorrhaphy, or thoracotomy BEE × 1.4
Severe Major bowel perforation with resection, major open wounds,
intraabdominal abscess BEE × 1.6

Table 8-4. KCAL / KG GOALS

Patient Feeding Level (kcal/kg) Level by Indirect Calorimetry
Normal weight patients 25-30 REE† × 1.0
Underweight patients 35-40 REE × 1.2
Obese patients 20-25* REE × 0.85
Morbidly obese 10-20* REE × 0.75

†Resting energy expenditure (REE) is the measure of energy expenditure in a fed state and is generally 10% higher than BEE.
*Use adjusted weight.

8. What is indirect calorimetry?

Show answer
It is a bedside test in which the patient’s production of carbon dioxide and consumption of oxygen are measured for approximately 30 minutes until steady state is achieved. Results are inserted into the modified Weir equation:

REE = [(3.796 x VO2) + (1.214 x VCO2)] x 1440 min/day

where REE = resting energy expenditure (kcal/day), VO2 = oxygen consumption (L/min), and VCO2 = CO2 exhaled (L/min).

The chart reports the number of kilocalories the patient is predicted to consume in 24 hours and the respiratory quotient (RQ). RQ = VCO2/VO2 and provides information on the type of substrate being used. The RQs for the metabolism of fat, protein, and carbohydrate are 0.7, 0.83, and 1.0, respectively. Overfeeding results in an RQ > 1.0.
KEY POINTS: RESPIRATORY QUOTIENT

1. Defined as ratio of CO2 produced to O2 consumed
2. Easy to perform on mechanically ventilated patients
3. Identifies principal metabolic substrate used by the patient
4. Ratio for fat (0.7), protein (0.83), and carbohydrates (1.0)
5. 5. Ratio < 1 indicates starvation or underfeeding; ratio > 1 indicates overfeeding, lipogenic status
6. Increased CO2 production linked to difficulty with ventilator weaning and impaired immune response

9. When is indirect calorimetry useful?

Show answer
The test may be performed on mechanically ventilated patients as soon as they are relatively stable, with a fractional concentration of oxygen in inspired gas (FiO2) < 60% and peak end-expiratory pressure (PEEP) < 10. Studies are helpful:

* When overfeeding (e.g., in diabetes mellitus, chronic obstructive pulmonary disease [COPD]) would be undesirable
* When underfeeding (e.g., renal failure, large wounds) would be especially detrimental
* In patients whose physical or clinical factors promote energy expenditure deviant from normal
* When drugs are used that might alter energy expenditure (e.g., paralytic agents, beta blockers)
* In patients who do not respond as expected to calculated regimens

Colorectal Carcinoma

admin — Thu, 09 Jul 2009 07:21:18 +0000

54 COLORECTAL CARCINOMA
Kathleen Liscum M.D.

1. What are the top three causes of cancer deaths in the United States?

Show answer
Lung, breast or prostate, and colon cancer.

2. List a few of the presenting symptoms of patients with colorectal cancer.

Show answer
Intermittent rectal bleeding, vague abdominal pain, fatigue secondary to anemia, change in bowel habits, constipation, tenesmus, and perineal pain.

3. What options are available to evaluate a patient who has guaiac-positive stools?

Show answer
To evaluate the entire colon and rectum, one may perform a barium enema and proctoscopy or a colonoscopy. Colonoscopy is 10 times more expensive but is more sensitive for lesions < 1 cm.

4. List at least five risk factors for colorectal cancer.

Show answer
Prior adenomatous polyps, family history of colorectal cancer, age older than 40 years, chronic ulcerative colitis, Crohn’s colitis, history of colon cancer, exposure to pelvic radiation for prostate or cervical cancer, and familial polyposis. Hamartomatous polyps (Peutz-Jeghers syndrome), inflammatory polyps, and hyperplastic polyps are not considered premalignant.

5. What are the current screening recommendations of the American Cancer Society for colorectal cancers?

Show answer
A yearly digital rectal examination with testing for occult blood for patients age 40 years and older. Additionally, for patients older than age 50 years, a flexible sigmoidoscopy is recommended every 3-5 years.

6. In what part of the colon or rectum are most cancers found?

Show answer
Historically, there has been a higher incidence of cancers in the rectum and left colon. However, over the past 50 years, there has been a gradual shift toward an increased incidence of right colon cancers. This change in pattern may reflect improvement in early detection.

7. Surgical options for colorectal cancer are dependent on the tumor location. What operation should be performed for a patient with a lesion at 25 cm from the anal verge?

Show answer
A sigmoid colectomy.
8. What about a lesion at 9 cm from the anal verge? Show answer
A low anterior resection (LAR).
9. What about a lesion at 4 cm from the anal verge? Show answer
An abdominoperineal resection (APR). This requires a permanent colostomy.

10. What is the significance of finding adenomatous polyps in a patient’s colon?

Show answer
KEY POINTS: COLORECTAL CARCINOMA

1. Presenting symptoms may include intermittent rectal bleeding, vague abdominal pain, fatigue secondary to anemia, change in bowel habits, constipation, tenesmus, and perineal pain.
2. The current recommendations of the American Cancer Society for screening are a yearly digital rectal exam with testing for occult blood at age 40 years and for patients over 50 a flexible sigmoidoscopy every 3-5 years.
3. Patients with lymph node involvement should receive chemotherapy postoperatively to treat micrometastases.

This patient is six times more likely to develop colorectal cancer than a patient without polyps. Evidence suggests that all colon cancers arise from adenomatous polyps. The “adenoma-carcinoma sequence” describes this transformational process. Patients with familial adenomatous polyposis (FAP) typically harbor more than 100 polyps, which cover the colonic mucosa. If these patients go untreated, they will, without exception, develop adenocarcinoma of the colon by age 40 years.

11. How does the surgeon prepare the patient’s colon for an operation?

Show answer
Bowel preparation includes both a mechanical cleansing and appropriate antimicrobial prophylaxis. This combination has resulted in significant decrease in morbidity and mortality from colon surgery. Mechanical cleansing can be accomplished by lavage with polyethylene glycol (Go-Lytely) or a combination of cathartics and enemas (Fleet’s Prep).
Antimicrobial prophylaxis should cover the expected aerobic and anaerobic flora of the gut. Significant controversy exits over whether the antibiotics should be given enterally (e.g., neomycin, 1 g, and metronidazole [Flagyl], 1 g, three times orally at 4-hour intervals the evening before surgery) or parenterally (e.g., cefotetan, 2 g intravenously within 1 hour before surgery). Many clinicians give both to obtain both intraluminal and systemic protection.

12. What is Dukes’ staging system?

Dukes A – Tumor confined to bowel wall
Dukes B – Tumor invading through the bowel wall
Dukes C – Tumor cells found in the regional lymph nodes

In 1932, Dr. Dukes described a staging system for rectal cancer. He originally described the following: Since his original article was published, this classification has been modified several times. One of the most commonly used modifications is the inclusion of Dukes’ D stage, which indicates distant metastases.

13. Which patients with colorectal cancer require adjuvant (postoperative) therapy?

Show answer
Patients with lymph node involvement (Dukes’ C) should receive chemotherapy postoperatively to treat micrometastases. Two large studies have documented a survival advantage for these patients. However, no studies have documented a survival advantage for patients with Dukes’ B disease treated with chemotherapy.
Patients with rectal cancer with a significant chance of local recurrence (Dukes’ B and C) should be treated with radiation therapy. This may be given preoperatively, postoperatively, or with a combined “sandwich” technique.

References
WEB SITE
http://www.nejm.org
BIBLIOGRAPHY
1. Colorectal Cancer Collaborative Group: Adjuvant radiotherapy for rectal cancer: A systematic overview of 22 randomised trials involving 8507 patients. Lancet 358:1291-1304, 2001.
2. Jass JR: Pathogenesis of colorectal cancer. Surg Clin North Am 82:891-904, 2002. Medline Similar articles
3. Levin B, Brooks D, Smith RA, Stone A: Emerging technologies in screening for colorectal cancer: CT colonography, immunochemical fecal occult blood tests, and stool screening using molecular markers. CA Cancer J Clin 53:44-55, 2003. Medline Similar articles
4. Lynch HT, de la Chapelle A: Hereditary colorectal cancer. N Engl J Med 348:919-932, 2003. Medline Similar articles
5. National Institutes of Health Consensus Conference: Adjuvant therapy for patients with colon and rectal cancer. JAMA 264:1444-1450, 1990.
6. Ransohoff DF: Screening colonoscopy in balance issues of implementation. Gastroenterol Clin North Am 31:1031-1044, 2002. Medline Similar articles
7. Salz LB, Minsky B: Adjuvant therapy of cancers of the colon and rectum. Surg Clin North Am 82:1035-1058, 2002.
8. US Multisociety Task Force on Colorectal Cancer: Colorectal cancer screening and surveillance: Clinical guidelines and rationale-update based on new evidence. Gastroenterology 124:544-560, 2003.

Cardiopulmonary Resuscitation

admin — Mon, 06 Jul 2009 19:02:23 +0000

2 CARDIOPULMONARY RESUSCITATION
Norman A. Paradis M.D., Alden H. Harken M.D.

1. Define sudden cardiac death.

Sudden ventricular fibrillation (VF) or pulseless electrical activity (PEA). Acute coronary ischemia and preexisting cardiac disease are the most common causes. VF is becoming less common.

2. What is the predominant determinant of successful cardiopulmonary resuscitation (CPR)?

Show answer
Time to restoration of spontaneous circulation, which itself is a function of the time to effective chest compression and time to defibrillation of VF. The chance of a good outcome decreases by 10% per minute. Successful outcomes are more likely if CPR is initiated promptly and if preexisting hypothermia is present.

3. What are the ABCs?

Show answer
Airway, breathing, and circulation. But things have changed. There are now three recognized phases of CPR: electrical, mechanical, and metabolic.

1. The electrical phase lasts about 5 minutes-during that phase, only immediate electrical cardioversion may be required.
2. The mechanical phase lasts 5 to 10 minutes after onset of arrest-during this phase, a few minutes of chest compression are required before cardioversion.
3. The metabolic phase begins at 10 minutes postarrest. During this phase, pressor and antiarrhythmic drugs are required.

4. How do you electrically cardiovert (shock) a patient?

Show answer
Gel pads now are more common than hand-held paddles. If you are using paddles, place electrolyte (conductive) gel on them. Place one pad or paddle in the right subclavicular area and the other in the midaxillary line at the level of the eighth intercostal space (over the apex of the heart). If you are using a biphasic defibrillator, the fist shock should be only 100 J. With monophasic defibrillators, start at 200 J. If the patient remains in VF, rapidly increase the output to the maximum the machine allows. Take care to confirm that everyone (including you) is clear before delivering a shock.
5. Is there an immediate need for an airway? Show answer
No. Defibrillation and chest compression should be initiated first. Waiting for intubation to be completed before initiation of these interventions is one of the most common mistakes in advanced life support. Children, in whom primary respiratory arrest is more common, are an exception. Restoration of ventilation in children often reveals that pulselessness was severe shock, not cardiac arrest.

6. How do you establish an airway-even in a patient with suspected neck injury?

Show answer
The three basic maneuvers are head tilt, chin tilt, and jaw thrust. In an unconscious patient, the jaw muscles relax. The jaw thrust subluxes the mandible, pulling the tongue and epiglottis anteriorly off the upper airway (with minimal cervical hyperextension).
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7. Is endotracheal intubation mandatory?

Show answer
No.

* Mouth-to-mouth ventilation delivers 16% inspired oxygen.
* Bag-mask ventilation delivers 21% oxygen.
* Bag-mask ventilation with an oxygen supply can deliver close to 100% oxygen.

8. Name the advantages of endotracheal intubation. Show answer
A relatively secure airway. Mouth-to-mouth or bag-mask can deliver significant amounts of air to the stomach. Gastric distention impairs diaphragmatic movement and may predispose to aspiration.

9. Does an endotracheal tube (even with the cuff up) prevent aspiration?

Show answer
No. If you place a couple of drops of methylene blue on the tongue of an intubated patient, you can suction “blue” from the other end of the tube (beyond the cuff) within 90 seconds.

10. Which size endotracheal tube should you use?

Show answer
Select a tube with an internal diameter equal to the width of the patient’s little finger. For a 70-kg adult, a 7.5-mm tube is fine. Do not delay ventilation trying to place a large endotracheal tube. Adequate ventilation can be achieved through smaller tubes.

11. How do you know if the endotracheal tube is in the proper position?

Show answer

1. Listen to both lung fields.
2. Observe symmetric chest excursion with each tidal breath.
3. Listen over the epigastrium (you don’t want to hear gurgles from the stomach).

These physical findings are not fully reliable, however. In patients with spontaneous circulation, it is now standard to confirm tube placement with end-tidal CO2 (ET-CO2) measurement. In cardiac arrest, even ET-CO2 may be unreliable. You should confirm tube position as soon as possible by chest x-ray.

12. Which is preferred-oral or nasal intubation?

Show answer
Oral intubation. You can watch the tube pass directly through the vocal cords, ensuring proper placement. Nasal intubation is a blind technique, relatively contraindicated in patients with maxillofacial trauma (because of the risk of intracranial placement of the tube through an anterior fossa fracture) and in patients with known or suspected coagulopathy (because nasal mucosa is well vascularized, intubation may cause major epistaxis). Oral endotracheal intubation with “in-line” neck stabilization is preferred even in patients with suspected neck injury.

13. What is the role of an esophageal obturator airway (EOA)?

Show answer
None. At present, the EOA is not indicated because alternative techniques (mask or endotracheal tube) are safer and more effective.

14. What should be your first consideration if you are unable to ventilate or intubate a patient?

Show answer
Foreign body airway obstruction. Attempt to visualize the foreign body directly, and remove it with either suction or Magill forceps.

15. Explain the proper method of external chest compression.

Show answer
Place the patient on a firm surface-typically the floor or on a backboard. The rescuer should be positioned beside the patient’s chest. Both hands are placed just above the xiphoid-sternal junction. Keep your arms straight and your shoulders directly over the patient’s sternum. The compression depth should be 4-5 cm. Use the weight of your upper body to achieve adequate depth of compression. Perform 15 compressions followed by 2 ventilations at a rate of 100 compressions/minute.
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16. What are the essentials of external chest compressions?

Show answer
Even performed properly, external chest compression produces only a fraction of normal vital organ blood flow. Coronary blood flow occurs only during the release phase. Most providors do not use adequate force-make sure that the chest is compressed at least 2 inches in adults. Interruption in chest compression (to check the ECG rhythm or pulse) significantly reduces the efficacy of CPR.

17. What are the complications of external chest compressions?

Show answer
Complications are common but not important. Rib and sternal fractures occur 80% of the time. Major cardiac or pericardial injuries (lacerations) are rare. Bone marrow and fat emboli are common (80% in one series). Do not let fear of complication interfere with effective chest compression.

18. What are the indicators that effective CPR is being performed?

Show answer
Real-time indicators of vital organ perfusion are lacking. Effective CPR and pressor drugs should cause the VF waveform amplitude to increase-so called coarsening. Improved cerebral perfusion may result in gasping. During CPR, ET-CO2 > 15 mmHg predicts return of spontaneous circulation. Switch chest compression providers if the ET-CO2 begins to fall because this may indicate fatigue of the rescuer.

19. Is the central line the best access to the circulation?

Show answer
Yes. Large volumes of fluid can be delivered to the venous system more quickly, however, via large-bore peripheral venous catheters. A 14G, 5-cm catheter (peripheral) can deliver twice the flow of a 16G, 20-cm catheter (central). Central line placement may be associated with significant complications, including pneumothorax, air embolus, and arterial puncture. In hypo-volemic patients, in whom central veins are collapsed and peripheral veins are constricted, venous cannulation can be difficult.

20. Does a central line offer therapeutic and diagnostic advantages?

Show answer
Yes. A central line permits bolus administration of drugs to the right side of the heart. Identification of a high central venous pressure may indicate the need to treat reversible causes of PEA, such as cardiac tamponade or tension pneumothorax.

21. Is it necessary to monitor arterial blood gases during resuscitation?

Show answer
No. After you have an adequate airway and presumably are delivering 100% oxygen, you don’t care what the arterial PO2 is because you can do nothing about it. If possible, you may confirm the adequacy of oxygenation on the arterial side through an early arterial blood gas. Then you should focus on the adequacy of chest compression.

22. Which is preferred-colloid or crystalloid resuscitation fluid?

Show answer
Colloid advocates claim that the big molecules remain in the intravascular space and are more effective in elevating blood volume. Crystalloid advocates state that capillaries leak albumin, especially in the shock state. Resuscitation with crystalloid is clearly safe. Given its availability, low cost, and safety, crystalloid (lactated Ringer’s solution) is the choice for initial fluid resuscitation. When true cardiac arrest has occurred, however, volume is of little importance.

23. In a patient exhibiting asystole, bradycardia, PEA, or fine fibrillation, what is your primary goal?

Show answer
Adequate vital organ perfusion, especially to the coronary arteries. Done properly, CPR may cause PEA to progress to stable hemodynamics or VF to become “coarse enough” for successful countershock.
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24. Summarize the reversible causes and treatment of PEA.

Show answer
PEA is an orderly electrical rhythm in the absence of detectable arterial pulses. The potentially correctable situations that commonly cause electromechanical dissociation (EMD) are:

1. Tension pneumothorax (diagnosis: hyperresonant chest, decreased breath sounds), treated by decompressing the pleural space on the side of the collapsed lung
2. Pericardial tamponade (diagnosis: Beck’s triad-distant heart sounds, distended neck veins/elevated central venous pressure, and hypotension), treated with pericardiocentesis
3. Hypovolemia, treated with volume replacement
4. Pulmonary embolism, treated with fibrinolysis
5. Pump failure secondary to massive myocardial infarction, treated with fibrinolysis or mechanical assistance (intra-aortic balloon pump)
6. Hyperkalemia, treated with calcium and bicarbonate

KEY POINTS: REVERSIBLE CAUSES OF PEA

1. Tension pneumothorax
2. Pericardial tamponade
3. Hypovolemia
4. Pulmonary embolism
5. Pump failure
6. Hyperkalemia

25. Is clinical PEA always full cardiac arrest?

Show answer
PEA is a heterogeneous entity with hemodynamics ranging from full cardiac arrest through normal blood pressure. Confirm true cardiac arrest as early as possible through echocardiography or placement of an arterial catheter.

26. Name the most common cause of cardiac arrest in the perioperative period.

Show answer
Although the incidence of VF is increased in the perioperative period, PEA secondary to potentially reversible insults is more common at this time.

27. List the drugs commonly used during resuscitation and the appropriate dosages.

Show answer
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1. Oxygen: to reverse hypoxia, always provide 100% oxygen initially.
2. Epinephrine: α- and β-adrenergic agonist. IV dose is 5-10 mL of 1:10,000 solution. Because of the short duration of action, a repeat dose may be necessary after 5 minutes. Epinephrine is inactivated by alkali; do not mix with bicarbonate solutions. Although it enhances myocardial performance, epinephrine greatly increases myocardial oxygen demand. Ventilate!
3. Vasopressin: antidiuretic hormone-a new first-line pressor during cardiac arrest. Administer one time as a bolus of 40 U.
4. Amiodarone: first-line, broad-spectrum antidysrhythmic possibly useful in treating VF/ventricular tachycardia (VT) cardiac arrest and atrial arrhythmias. It is active at cardiac sodium, potassium, and calcium channels and has a- and b-adrenergic blocking properties. In cardiac arrest, it is administered as a 300-mg rapid IV infusion. Amiodarone may cause hypotension and bradycardia; a pressor drug, such as epinephrine or dopamine, should be readily available or already administered.
5. Atropine: parasympatholytic (vagolytic) agent that increases the discharge rate of the sinus node. Atropine is useful in treating sinus bradycardia associated with hemodynamic compromise. An IV dose of 0.5 mg is repeated at 5-minute intervals until a desirable rate is achieved (at least 60 beats/min). Increased heart rate increases myocardial oxygen demand; atropine should be used only if the bradycardia causes hemodynamic compromise (heart rate, 60 beats/min).
6. Dopamine: catecholamine precursor of norepinephrine active at dopaminergic receptors. Stimulates the heart and vasoconstricts (high dose) the periphery. Use as a vasopressor to treat hypotension secondary to bradycardia or decreased peripheral vasomotor tone. Dosage should be adjusted based on clinical end points starting at 2-5 μg/kg/min up to 20 μg/kg/min. The principal toxicity, seen with prolonged dosages > 10 μg/kg/min, is splanchnic and systemic vasoconstriction with resultant injury.
7. Dobutamine: synthetic catecholamine that is a cardiac b-receptor agonist used to treat cardiogenic shock. It increases cardiac contractility. Reflex peripheral vasodilation may require combination with a pressor drug, such as dopamine. Dosage should be adjusted based on clinical end points starting at 5 μg/kg/min up to 20 μg/kg/min.
8. Sodium bicarbonate (NaHCO3): no longer commonly used in cardiac arrest; in shock, it is used to reverse acidosis (hypoxia-induced anaerobic metabolism leads to acid accumulation). The initial dose is 1 mEq/kg. One ampule (50 mL) contains 50 mEq of sodium bicarbonate. Bicarbonate combines with hydrogen ions to form CO2 and water; adequate ventilation is required for bicarbonate therapy to be fully effective. Overzealous use of bicarbonate may result in hypernatremia/hyperosmolality (each HCO3- is accompanied by a sodium ion).
9. Magnesium: effective in treating drug-induced torsades de pointes or VT. Administer 1-2 g IV over 3-5 minutes. May cause hypotension.
10. Calcium chloride or gluconate: positive inotropic agent. Calcium ions bind to troponin (the cardiomyocyte-specific calcium regulatory protein used to diagnose an acute myocardial infarction), which enhances the formation of cross-bridges between muscle contractile filaments with resultant fiber shortening. Dose is calcium chloride (or gluconate), 500 mg IV push. Do not mix with bicarbonate because it will precipitate.
11. Lidocaine: local anesthetic that suppresses ventricular arrhythmias (automatic and reentrant; see Chapter 3). An IV bolus of 1 mg/kg is followed by IV infusion at 2-4 mg/min. An additional IV bolus can be given at 10 minutes after initial dose if arrhythmias persist. Amiodarone is accepted as a preferred agent for treatment of arrhythmias.
12. Adenosine: a naturally occurring vasodilating hormone that is synthesized by vascular endothelial cells and dramatically slows artrioventricular (AV) nodal conduction. It is useful in the therapy of supraventricular tachyarrhythmias. Dose is 6 mg or 12 mg injected in a rapid IV bolus (which may be repeated several times). The half-life of IV adenosine is only 12 seconds. Measurable systemic hypotension occurs in < 2% of patients because adenosine is metabolized before it reaches the systemic vessels.
13. Verapamil: slow-channel calcium blocker used to block the AV node and to treat paroxysmal supraventricular tachycardia that causes hemodynamic compromise. Dose is 0.1 mg/kg. Dilute drug with 10 mL of saline, and infuse 1 mL/min until the supraventricular tachycardia either breaks or blocks. Repeat dose after 30 minutes if not effective. The drug reduces systemic vascular resistance and may cause hypotension.

28. What measures should be considered postresuscitation to improve the chances of a good outcome?

Show answer
Laboratory and clinical data support use of mild hypothermia (34°C for 24 hours)in patients who remain comatose after resuscitation from cardiac arrest. Hypotension or causes of increased cerebral oxygen use (e.g., as seizures or fever) should be treated aggressively.

References
WEB SITE
http://www.americanheart.org/presenter.jhtml?identifier=10000056#P
BIBLIOGRAPHY
Harken AH: Cardiac dysrhythmias. In Wilmore DW, Cheung L, Harken AH, et al (eds): Scientific American Surgery. New York, Scientific American, 1999.

Queries 4

admin — Fri, 14 Aug 2009 18:13:50 +0000