	Universidad Iberoamericana School of Medicine

	Infectious Diseases and Critical Care Medicine

: Pneumoperitoneum (PP) secondary to blunt abdominal trauma is rarely observed in adults whose viscus has not ruptured. The condition is encountered even less frequently in blunt thoracic trauma patients, who are more likely to present with pneumothoraces, pneumomediastinum, or pneumopericardium.

: Because of the increased use of computed tomography and its high sensitivity, PP often may be an incidental finding in blunt trauma patients. The authors report one such case in a patient who was thrown off his motorcycle when it collided with a motor vehicle. The patient had PP although his viscus did not rupture. The authors provide a comprehensive discussion on the etiology of PP and provide insights on how it may occur in the absence of a ruptured viscus.

: Complications from missed intra-abdominal injuries can be disastrous; thus, once PP is identified, exploratory laparotomy is almost always warranted. If a patient?s PP is thought to originate from a benign cause and conservative management is elected, the patient?s vital signs must be monitored closely and serial examinations of the abdomen must be undertaken along with frequent laboratory evaluations.

	Pneumoperitoneum (PP) is a striking radiological finding that is almost always indicative of severe intraabdominal disease. It is generally accompanied by prominent clinical symptoms and physical findings consistent with peritonitis, and the need for immediate surgical intervention is apparent. Ninety percent of PP cases result secondary to a perforated viscus and demonstrate intraperitoneal free air on radiography.

 The remaining 10% of cases are attributable to a variety of nonpathologic causes that result in free subdiaphragmatic air but may not require surgical intervention. Such cases have been referred to as "idiopathic" or "spontaneous" PP.

 The origin of air in these cases generally can be attributed to air leakage from pneumatosis cystoides intestinalis,

 a minute leak from a colonic diverticulum,

 insufflation of air through the female genital tract,

	Another type of idiopathic PP, which is far rarer, is associated with pneumothorax secondary to trauma.

 In these cases, thoracic air is introduced through a rupture of the lungs and dissects retroperitoneally or leaks directly through defects in the diaphragm.

 The diagnosis of PP in this group of patients does not invariably mean gastrointestinal perforation and, therefore, does not always require operation. Conservative management with prudent judgment and meticulous observation may avoid unnecessary surgery in these patients.

	A 24-year-old man was riding a motorcycle when he collided with a sports utility vehicle and sustained major injuries. While being transported to the hospital by emergency medical services, he developed significant respiratory distress. A needle thoracocentesis was performed on the right side for tension pneumothorax, which promptly improved his symptoms. On arrival to the emergency department, he underwent placement of a chest tube on the same side as the needle decompression.

	The patient was initially hypotensive, with a blood pressure of 88/55 mm Hg (normal, 100-to-119/60-to-79 mm Hg). After resuscitation with crystalloids, his systolic blood pressure improved to 120 to 130 mm Hg, but he remained tachycardic. There were no lateralizing neurologic signs, and he scored a 15 on the Glasgow coma scale (a score of 13 to 15 indicates mild head trauma, whereas a score of 3 to 8 indicates coma). An admission hemogram, urinalysis, and blood chemistries were within normal limits. A bedside transthoracic echocardiogram showed normal systolic function without wall-motion abnormalities.

	A computed tomography (CT) scan of the patient's chest showed multiple rib fractures bilaterally, bilateral pulmonary contusions, bilateral pneumothoraces, extensive right chest wall subcutaneous emphysema, and a sternal fracture (Figure 1). Pneumomediastinum and pneumopericardium were observed. The great vessels and the tracheobronchial tree were intact. There was no evidence of hemothorax. A CT scan of the abdomen and pelvis showed a splenic laceration and PP without any other intraabdominal or intrapelvic injuries (Figure 2). The decision was made to perform an urgent exploratory laparotomy to rule out injury to a hollow viscus.

	A left-sided chest tube was placed, and the patient was brought to the operating room, where he was intubated and ventilated. Intraoperatively, the patient was found to have a large abdominal wall injury in the right upper quadrant just below the diaphragm, with an adjacent nonexpanding retroperitoneal hematoma and a small mesenteric hematoma. The splenic hilum was disrupted and actively bleeding, necessitating a splenectomy. Careful inspection of the viscera did not reveal any evidence of bowel perforation and the diaphragm was found to be intact. The extrahepatic biliary tract was uninjured.

	The patient's postoperative recovery was complicated by acute respiratory distress syndrome and persistant pneumothorax on the right side. He was discharged from the hospital in good condition on postoperative day 14.

	PP is an alarming radiographic finding that is almost always pathognomonic of a ruptured viscus and usually requires immediate exploratory laparotomy. In cases of blunt chest or abdominal trauma, CT scanning is a mandatory part of the evaluation; however, it is not known whether finding free intraperitoneal air on the CT scans of a trauma patient reliably indicates gastrointestinal perforation. In a series by Kane and colleagues, CT scanning was done routinely in evaluating blunt abdominal trauma patients, and free air was associated with a ruptured viscus only 22% of the time.

 The clinical significance and outcomes of CT-detected PP in blunt trauma patients raises two questions: What is the pathophysiology of CT-detected PP in the setting of blunt chest or abdominal trauma with no evidence of bowel perforation? And, what management protocol should be followed for blunt trauma patients after PP is detected with CT scanning?

	The association between pneumothorax and idiopathic PP has been reported in several case studies of patients who have sustained blunt trauma.

 In the study by Kane and colleagues, pneumothorax was found in 50% of blunt trauma patients with CT-detected PP.

 None of these patients had bowel perforation. Because intraabdominal pressure exceeds intrathoracic pressure by an average of approximately 20 to 30 cm H

O during both inspiration and expiration, 18 simple pneumothorax should not lead to PP. Even patients with tension pneumothorax develop this complication infrequently due to the rapidity of treatment or inadequate buildup of intrathoracic pressure.

 These findings suggest that very high intrathoracic pressure is required to cause dissection of air through the retroperitoneal space.

	Speculation on the etiology of PP without pneumothorax

	No definitive explanation exists for the presence of PP in blunt trauma patients without concomitant pneumothorax. The speculation is that the free intraabdominal air in these patients may have resulted from intestinal microperforations, which rapidly seal and leave behind no obvious clinical sequelae. This is akin to the well-described clinical entity of pneumatosis cystoides intestinalis, which is a rare cause of PP after blunt abdominal trauma.

 In this syndrome, airfilled sacs develop in the bowel wall as a result of mucosal microperforations through which air transects into the intestinal serosa.

 Intraperitoneal free air results when these sacs rupture.

	The association of mechanical ventilation with pneumothorax increases the risk of air dissection into the peritoneal cavity. Laboratory experiments by Grosfeld and associates in the early 1970s show that interstitial emphysema develops when intratracheal pressures exceed 40 cm H

 Pneumomediastinum develops at pressures of 50 cm H

O, and subcutaneous emphysema accompanied by PP can appear at pressures of 60 cm H

O and greater. It is thought that air leaking from ruptured alveoli collects in the interstitial space. As intrathoracic pressure increases, the air dissects along the sheath of adjacent vessels into the mediastinum. The air can then dissect into various spaces, including the pleural space and along the thoracic great vessels and esophagus into the retroperitoneum, where it may rupture into the peritoneal cavity and cause PP.

	Other literature shows that overinflation of the lungs with high ventilatory pressures can cause air to dissect along the esophagus and aorta, resulting in pneumoretroperitoneum.

 After conducting seminal experiments in 1937, Macklin concluded that air leaking from ruptured alveoli travels along the perivascular sheaths of the mediastinum and retroperitoneum, ultimately reaching the peritoneal cavity and causing PP.

 Alveoli rupture most commonly occurs around the kidneys.

 Operation is not deemed necessary in these cases.

	Some posttraumatic patients with pneumothorax developed PP following mechanical ventilation.

 This likely resulted when air dissected into the peritoneum. The studies by Macklin and later by Grosfeld and associates demonstrate how high intratracheal pressure and overinflation of the lungs can cause pneumoretroperitoneum and subsequent PP.

 It seems that in patients on mechanical ventilation, especially those with pneumothorax and subcutaneous emphysema, the appearance of free intraperitoneal gas does not necessarily indicate a surgical emergency.

			A radiographic finding of pneumoperitoneum (PP) is almost always pathognomonic of a ruptured viscus.

			In trauma patients with concomitant PP, pneumothorax, and pneumomediastinum, CT findings of free peritoneal fluid and mesenteric or bowel wall thickening indicate a surgical emergency.

			PP in patients on mechanical ventilation, especially those with pneumothorax and subcutaneous emphysema, often can be treated conservatively.

	The blunt trauma patient described in our case report developed bilateral pneumothoraces, pneumomediastinum, and PP. There was no clinical evidence of a perforated viscus, and he was not being mechanically ventilated. The patient's pneumothoraces were thought to be due to his fractured ribs. High intrathoracic pressures forced air into the abdomen either directly across a defect in the diaphragm or indirectly through the mediastinum retroperitoneally. Rupture of the diaphragm, which is an unusual injury following blunt abdominal trauma, must be suspected in all patients with massive trauma.

 Our patient's clinical picture and imaging studies, along with a careful examination of his diaphragm during exploratory laparotomy, did not show diaphragmatic rupture. One plausible explanation of his PP is that very high intrathoracic pressure following the initial impact caused bilateral pneumothoraces and pneumomediastinum, leading to dissection of air through the mediastinum into the retroperitoneum and, finally, to the peritoneal cavity. The high pressure of the tension pneumothorax was treated by emergency medical services and again in the emergency department; thus, our patient's PP most likely occurred on impact or immediately thereafter.

	The dilemma for surgeons is deciding whether CT-detected PP in posttraumatic patients with concurrent pneumothorax is attributable to a benign abnormality or whether it indicates a potential surgical emergency. In the study by Kane and colleagues, approximately 80% of blunt trauma patients with CT-detected PP did not have an abdominal injury requiring surgery; however, the series in this study was too small to make a legitimate statistical analysis.

	When there is a question as to whether an operation is warranted in a trauma patient with pneumothorax, pneumomediastinum, and CT-detected PP, the CT findings need to be assessed very carefully. CT findings that mandate a trip to the operating room include free peritoneal fluid and mesenteric or bowel wall thickening. If CT findings are questionable and conservative treatment is elected, then serial examinations of the abdomen (preferably by the same clinician), frequent laboratory examinations, and constant monitoring of vital signs must be undertaken.

Articles

Surgical Rounds

Ilya Sabsovich, MD, Elmhurst Hospital Center, Elmhurst, NY, and Mount Sinai School of Medicine, New York, NY; Ravi Desai, MD, Mount Sinai School of Medicine, New York, NY; Rafael Alba, MD, Universidad Inberoamericana School of Medicine, Santo Domingo, Dominican Republic; Jose Yunen, MD, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY; and David Sammett, MD, Elmhurst Hospital Center, Elmhurst, NY

Idiopathic pneumoperitoneum after blunt chest trauma

By Lawrence A. Danto, MD, and Valeria Kelly

	We've all had them. They arrive with an agenda that goes beyond securing appropriate care. They are unknowingly—or uncaringly&mdash;disruptive. They prefer to share what they have learned about their condition from friends and Websites rather than hear what you have learned from years of training and experience about the best way for them to recover. They imagine their problems outweigh anything else happening in your practice. Their inflated sense of self-importance seems to loom even larger than the importance of their health.

	When encountering these difficult patients, we may respond as though they choose to be difficult, but often they cannot help behaving as they do. They act this way because their personal and medical histories have sent them in an emotional free-fall, and they are attempting to regain control over their lives by controlling others. As skilled professionals, we want nothing more than to see all our patients treated successfully. This requires learning to manage the problems unique to 'difficult' patients. More than a pill or an operation, they need help re-establishing a sense of control over their health. They need assurance that we empathize with their desire to become healthy and in control.

	Fortunately, difficult patients do not come along every day, but when they do, what is the best way to manage them? First and foremost, the difficult patient requires us to exercise patience, with them and ourselves. This is not always easy for a highly sought-out specialist, but there are steps you can take to handle difficult patients more effectively:

		Remind yourself that the difficult patient is fearful and deals with this fear by attempting to exert control over others.

		Understand and accept that difficult patients cannot change in the short-term.

		Allot difficult patients extra time, empathy, and accommodation.

		Train your staff to recognize, understand, and empathize with the difficult patient.

		If your staff suspects that a patient is 'difficult,' ask that they notify you before the appointment and allow extra time for the consultation.

		Instruct your staff to remain courteous to even the most difficult patients.

		Advise difficult patients that the consultation process begins as soon as the appointment is scheduled and may take longer than expected.

		Reassure them that they own their medical records but it is important to leave them with you for review until the process is completed.

		Explain that office routines are for more than convenience and exist to ensure patient safety and improve outcomes.

		Emphasize that you are committed to their care, but for the benefit of all patients, appointments should not be prolonged unnecessarily.

		Remain communicative and pleasant, no matter how uncommunicative or unpleasant they sometimes act.

		Be humble and remain patient. You will be surprised how well difficult patients respond once they are confident that you care and are receptive to their concerns.

	Surgeons sometimes err in assuming responsibility for ensuring an optimal outcome rather than relegating themselves to providing the best care they can offer irrespective of outcome. Because the patient's contribution is essential to achieving the best outcome, results are something we cannot and should not guarantee, especially when dealing with a difficult patient.

	In the end, we surgeons would do well to remember that all patients are potentially difficult and need us to care about them as people even more than we care about them as patients. No matter what, we must remember 

: a patient should never be mistreated. It is below the standard of care for a professional to lose the confidence and trust of even the most difficult patients—it hurts them and us. The mark of a true professional is to deal successfully with every patient. No one said it would always be easy.

	When it comes to blood, how old is too old? A recent study published in the 

 evaluated 6,002 heart surgery patients who underwent blood transfusions during surgery and determined that those who received blood that was more than 14 days old were more likely to experience complications or die. A total of 3,130 patients received the older blood, and the remaining 2,872 were transfused with blood that had been stored 14 days or less. The in-hospital mortality rate for patients receiving blood older than 2 weeks was 2.8% compared with 1.7% for patients who received fresher blood. Patients receiving the older blood also experienced longer periods of mechanical ventilation and increased rates of blood poisoning and kidney failure. This corresponds to a Duke University Medical Center study published in 2007, which found that red blood cells begin losing nitric oxide as soon as the blood leaves the donor's body. Nitric oxide is needed to keep blood vessels open so that the cells can enter tissues and deliver oxygen. Organs that are insufficiently oxygenated are more likely to fail.

	Recognizing that blood degrades, the Food and Drug Administration (FDA) established 42 days as the maximum time limit for storing blood, but ongoing nationwide shortages of blood result in most of it being used within 15 days of donation. Dr. Colleen Gorman Koch, lead author of the Cleveland Clinic study in 

, believes that "Blood should be classified as outdated earlier than current recommendations." FDA officials are not so sure and point out that the study, while interesting, was "narrow and non-randomized," and they are calling for more "definitive scientific information" before modifying blood storage procedures.

	Possible options for improving outcomes for heart surgery patients include limiting blood transfusions to emergency cases, recycling the patient's own blood, or administering drugs during surgery that minimize the likelihood a transfusion will be required. A companion editorial to the Cleveland Clinic study proposed another possibility: prioritizing blood supplies, reserving the freshest blood for cardiac patients and using older blood in those with low-risk conditions like anemia. Research is also underway to evaluate whether adding nitric oxide back to red blood cells prior to transfusion can improve surgical outcomes for cardiac patients.

	Approximately 43,000 pints of donated blood are used daily in the United States and Canada, but a growing list of restrictions on who can donate blood has cut into the amount of blood collected each year. Sixteen states sought to address this by lowering their donor age to 16, and legislation is pending to do the same in nine more states. It is worth noting that just one day after the terrorist attacks on September 11, 2001, the nation's blood supply was filled to capacity as 500,000 Americans donated blood. The easiest way to ensure that fresh blood is always available for heart surgery patients is for more Americans to roll up their sleeves more often.

	Six observations about sodium correction

	Sodium imbalances are common in hospitalized patients. Here are six interesting observations about sodium correction.

Normal saline is isotonic, yet it has 154 mEq/L of sodium.

		Blood plasma comprises 90% water and 10% cellular material. Normal sodium plasma levels average 140 mEq/L, which is the amount of sodium found in the liquid portion of plasma. To get a true concentration of sodium in a crystalloid solution, the 10% cellular component needs to be accounted for. This means that the normal sodium level of 140 mEq/L must be increased by 10%, or 14 mEq, for a total of 154 mEq/L, which is the level of sodium found in normal saline solution.

Hypokalemia needs to be corrected to correct for hyponatremia.

) is the predominant extracellular electrolyte, and potassium (K

) is the predominant intracellular electrolyte. Their concentrations are regulated by constant exchange using sodium potassium adenosine triphosphatase (ATPase) and reflect the relative proportions of solute and water and not the absolute amount of either solute or water. Plasma sodium concentrations are represented by the following equations:

		As these equations demonstrate, plasma sodium levels cannot improve unless the level of plasma potassium is corrected.

There are 154 ? 0.023 grams ≈ 3.5 grams of sodium in 1 L of normal saline solution.

		The atomic weight of sodium is 23.0 grams; thus, 1 mmol has 0.023 grams. Normal saline solution has 154 mEq/L of sodium because 1 mEq is equal to 1 mmol of sodium. It is important that clinicians know this, because many patients are kept on "maintenance fluids," which can add up to a lot of sodium when paired with the patient's normal diet.

The sodium concentrations in normal saline solution and Ringer's lactate are different.

		Normal saline solution has 154 mEq/L of sodium, and Ringer's lactate has 130 mEq/L of sodium. While the latter solution is used more commonly in surgical patients, the two fluids are nonetheless interchangeable for most purposes. It is important to remember that Ringer's lactate contains an additional 4 mEq/L of potassium and 28 mEq/L of lactate. Lactate is converted to bicarbonate in the liver and primarily helps in combating acidosis.

There are methods to estimate FENa in a patient on furosemide (Lasix).

		Fractional excretion of sodium (FENa) is commonly used to determine whether the etiology of a case of acute renal insufficiency is pre-renal or intrinsic; however, this calculation can have limited usefulness in patients who are on diuretics because these drugs interfere with sodium reabsorption. Several alternative calculations can be used, including calculating the fractional excretion of urea, uric acid, or lithium. All follow the same principle, which is that patient's in pre-renal states demonstrate avid salt and water reabsorption at the proximal tubule. Lithium, urea, and uric acid are also absorbed in the proximal tubule, but these are not affected by furosemide. The equivalents of FENa levels below 1% for lithium, uric acid, and urea are values lower than 15%, 12%, and 35%, respectively. Similarly, the equivalent of FENa levels above 1% for lithium, uric acid, and urea are values higher than 25%, 20%, and 35%, respectively. The fractional excretion of urea is thought to be the most sensitive and specific calculation in patients receiving diuretics.

It is generally not appropriate to use normal saline to treat hypernatremia.

		Hypernatremia frequently develops in hospitalized patients, and almost all cases are attributable to the loss or lack of free water. Iatrogenic salt excess due to intravenous fluids is commonly overlooked. When treating hypernatremia, hypotonic fluids like dextrose 5.0% in water (D5W), 0.2% normal saline, or 0.45% normal saline, are preferred unless the patient is hemodynamically unstable secondary to true volume depletion. If possible, oral supplementation or tube feeding of free water is preferable.

Dr. Kandula is an assistant professor of clinical medicine at Southern Illinois University School of Medicine in Springfield, IL.

	Imagine waking to find yourself unable to move or speak as someone cuts into your abdomen; imagine hearing a drill grinding through bone, smelling cauterized tissue, or feeling each needle-prick as your skin is stitched back together. While this scenario has all the makings of a gruesome nightmare, it is an extreme example of a rare but real phenomenon known as 

How to manage difficult patients, and more.

'Difficult' patients

	In the last year, as I traveled around the United States interviewing for a residency position, the question of why I chose America was put to me more times than I had anticipated. It was a staple in every interview; other times, it was asked by curious individuals I came across who had nothing to do with the residency program. With some discomfort, I had to dig deep into my life each time to try to find an answer for them.

	When I was a third-grade student, I attended boarding school in India. My friend Balwinder went to America and brought back a most remarkable pyramid of chocolate. It was as big as my young fist! I had never imagined a piece of chocolate so big to exist. Astonishingly, Balwinder had a whole line of those chocolate pyramids. He described his trip to visit his uncle in America, telling us all about his uncle's mansion, which had its very own swimming pool. He talked about the wide roads, the big cars, and his trip to Disneyland, where he met Mickey Mouse (who, he observed, was much taller than one would have expected). I vaguely remember that something twanged within my heart just then, for America had conquered me from the moment I first laid eyes on Balwinder's bar of Toblerone.

	In early middle school, paperback books became the rage. If I remember correctly, it was Ramswaroop who smuggled in the first Louis L'amour novel. In no time, the Wild West had been recreated in our little town of Lovedale in south India. The forested hillside of our school's large campus soon bore names like Dodge, Tombstone, Kansas City, and the whole area was referred to as Texas. Our free time was filled with talk of men and their reputations with guns, as well as reenacting shootouts. We were students by day and legendary gunmen by night. Vivid pictures of the rugged yet beautiful country described in those books were being etched, almost indelibly, in our imaginative minds. My heart silently yearned.

	When you leave a boarding school to rejoin the rat race that is the real world, a part of you dies. You wake up, your head leaves the clouds, your feet find the ground, and you start to run in the race without even realizing it. It is that small death and your performance in the race that the world celebrates as success, so I kept running—right into medical school. In those long days of classes, mud and grime from twice-daily bus rides, and late hours studying, I had little time to dream of anything at all, let alone America.

	In medical school, I decided that I was going to work hard, something I had not often done before, and I read all of the books I was assigned. There was a newfound joy in becoming knowledgeable. I noticed that America was more evident in medical school than ever before. Each subject came with a choice between two books: the cheaper, easier-to-understand, poorly presented abridged Indian version and the more complex, lavishly printed American textbook—the so-called "gold standard." In fairness, the Indian books never failed to convey all the information one needed; they were strewn with tables outlining all the causes of everything, from pallor to pericarditis. Yet, although they satisfied one's appetite for knowledge, they left me with a pervasive feeling of having done something sneaky, like I had taken a shortcut in a race. The American books encouraged me to read more; they made few assumptions and, when they did, they clarified them perfectly. In particular, they always seemed to me to answer the most important question: Why? I thought a lot about America and what it must be like to be a medical student there.

	I soon realized that, no matter how informative, all the textbooks were outdated, and one had to read journals to keep up with medicine. There again, overwhelmingly, I found America. Nearly every original article, most clinical trials, and almost every new drug came out of America. I started to wonder whether everything original was American. I nearly exploded my brain studying all the textbooks I could find so that I could get a residency position at one of the best hospitals in India. I hoped that the training I would get from practicing medicine there (evidence-based being the proclaimed fad) would prepare me for the 'real deal.'

	In my residency days, I silently endured a sense of helplessness, because nothing I had learned could be applied to the majority of patients I saw, who almost always faced a grim choice between bread for the family or treatment of their disease. In that argument, the former usually won convincingly. Even those who opted for treatment initially often quit midway due to their circumstances. Meanwhile, the resident was there at the patient's bedside as the patient died. The resident was well-read and could recite the latest guidelines off the top of his head, but, for reasons beyond the resident's control, he was unable to apply most of them. To the family, the resident was merely a bringer of bad news, a messenger of death.

	I thought the solution might lay in working among those who could afford what I had to offer, which would let me see firsthand whether everything that those books assured me would cure my patients' illnesses actually worked. After completing residency, I worked hard to pass a seemingly never-ending string of examinations, traveling by air, train, or greyhound bus as needed. My purse felt the pinch, and I exhausted the goodwill of distant relatives and old friends. All the while, I hoped that somewhere toward the end of this long road lay the beginning of my inspiration.

	Now, as I serve my internship in America, I have found over the last few months that it is less than my imagination sequentially built it up to be. I discovered that the Wild West exists no more (thankfully), the cold temperatures leave me feeling as though the blood in my bones will freeze, and snow only looks good in pictures, when it is undisturbed. I realized that the sizes of the cars do not matter if you do not own one and that poor people, at least relative to the cost of medical care, exist aplenty here and that often, paradoxically, they are obese. I have learned that one still has to look for inspiration but that the final words have not been spoken yet and I will learn more as I gain experience here. I also know that I am thankful I decided to make this journey, because otherwise I would have been dreaming about it all my life.

	Whenever someone asks me "why America," many pictures flash before my eyes as I try to gather my thoughts: a chunk of Toblerone, gunfights on the hillside, textbooks with fancy print, the 

, all the deaths that I haplessly pronounced. Despite this collage of images, I have never figured out how to put everything together during those brief encounters to fashion a reply that was even remotely eloquent. I sincerely hope that I have done so now.

Madhav C. Menon, MD, State University of New York, Syracuse, NY

Why America?

	These questions are similar to those asked on the American Board of Surgery Recertification Examination. Use them to prepare for the examination, fulfill learning requirements for various maintenance of competence programs, or simply improve your surgical knowledge. Answers can be viewed by following the "Read the Answers" link at the end.

		The most common cause of wound dehiscence is		

		All of the following signs are absolute indications for neck exploration after penetrating neck trauma, 

Is characterized by low creatine phosphokinase (CPK) levels

Requires alkalinization of the urine to solubilize myoglobin

Is best treated with diuresis induced by furosemide

		The nerve that runs along the spermatic cord and supplies sensation to the upper medial thigh is the		

		Carotid artery stenting for atherosclerotic occlusion		

Is indicated in patients who have undergone cervical radiation previously

Has the same stroke rate as endarterectomy

Has no effect on the contralateral carotid artery

Should not be performed in conjunction with coronary artery bypass graft surgery

		Preparation of a patient with sickle cell disease for elective laparoscopic cholecystectomy should include all of the following, 

Measures the expected success rate of liver transplantation

Determines the expected 3-month mortality rates without transplantation

Is less objective than the Child classification

Is highly dependent on the level of serum albumin

Can be distinguished from acute cholecystitis by the presence of jaundice

Is best treated using operative common duct exploration

Is a component of acalculous cholecystitis

Frequently cause diarrhea due to hypersecretion of vasoactive intestinal polypeptide (VIP)

Have a better prognosis if discovered before age 1 year

Are stage III if unresectable and associated with positive ipsilateral lymph nodes

Have the worst prognosis if the primary is in the mediastinum

Can be treated using ultrasonography-guided thrombin injection

Are best diagnosed using computed tomography

		All of the following are indications for operative therapy for bleeding duodenal ulcers, 

Persistent bleeding despite endoscopic therapy

Bleeding in a patient who has ischemic heart disease

Although chronic obstructive pulmonary disease, steroid use, ascites, and suture breakage predispose patients to wound dehiscence, overwhelmingly, the most frequent cause is a technical error, generally taking inadequate bites of fascia.

A large hematoma arouses concern, but operative exploration is absolutely indicated only if the hematoma is expanding. Venous injuries, which can create large hematomas, often stop bleeding spontaneously and do not necessarily require exploration. An open airway and subcutaneous emphysema suggest tracheal injury, which needs to be repaired. Pulsatile bleeding implies arterial injury, and exploration and vascular repair are necessary. Branham's sign is a manifestation of an arteriovenous fistula that needs to be repaired.

 Solubilization of myoglobin to facilitate its excretion is critical to protect the kidneys. Rhabdomyolysis is characterized by markedly elevated CPK levels and occurs after as few as 2 hours of ischemia. It is often worsened by reperfusion injury. Furosemide lowers urinary pH and is contraindicated. Saline infusion to induce diuresis is the most effective modality, with bicarbonate added to alkalinize the urine.

The iliohypogastric nerve is far cephalad and penetrates the quadratus lumborum. The ilioinguinal nerve runs along the spermatic cord and supplies sensation to the upper medial thigh. The obturator nerve passes beneath the iliac vessels. The genitofemoral nerve divides into the lumboinguinal nerve and the genital nerve, which supply the femoral triangle and the scrotal skin, respectively.

Radiation causes small vessel occlusion and wound problems; thus, stenting is preferable to endarterectomy. In low-risk patients, stenting is associated with a two-fold increase in stroke rate. Stenting puts the contralateral carotid artery at risk from the manipulation and instrumentation, and it does not prevent (rather, it facilitates) distal embolization on the ipsilateral side. Finally, it is the procedure of choice in patients with both coronary and carotid occlusion.

For patients with SS sickle cell disease undergoing extensive operations, exchange transfusion is indicated to lower hemoglobin S levels of <30% of total hemoglobin. It is not routinely indicated for those undergoing laparoscopic cholecystectomy. Alternatively, in very anemic patients, transfusion to a hemoglobin level of 10 g/dL may be used because administration of blood with 100% hemoglobin A dilutes the concentration of hemoglobin S. Hydration, normothermia, and oxygenation are all critical. Patients with sickle cell disease are somewhat immunosuppressed because of splenic infarcts; thus, prophylactic antibiotics are definitely indicated. In fact, many clinicians suggest maintenance of antimicrobial therapy for a minimum of 5 days postoperatively.

The MELD score is used to prioritize patients for liver transplantation by determining which ones are at greatest risk for early (3-month) mortality without transplantation. The MELD score is based on the international normalized ratio (INR) and serum creatinine and total bilirubin levels. The presence or absence of ascites and the serum albumin level are not factored into the calculation. Because the MELD score is quantitative, it is more objective than the Child classification. However, it does not predict survival after transplantation.

Cholangitis is caused by obstruction of the common hepatic duct or common bile duct and causes jaundice. In contrast, acute cholecystitis is caused by obstruction of the cystic duct, and although bilirubin levels may become minimally elevated, jaundice is not characteristic. The immediate need is for decompression of the bile duct (not cholecystectomy), which is best achieved by endoscopic retrograde cholepancreatography (ERCP). The mortality rate averages 2% to 5%. Acalculous cholecystitis is inconsistent with cholangitis, because no stones are present to obstruct the bile duct.

VIP-mediated watery diarrhea syndrome is a common paraneoplastic syndrome caused by neuroblastomas. Only 20% to 25% of neuroblastomas occur in the mediastinum, and these lesions have the best (not worst) prognosis. As described, these lesions are stage II. For a neuroblastoma to be classified as stage III, it needs to extend across the midline or be associated with positive contralateral lymph nodes. The prognosis is excellent if the lesion is discovered before (not after) the patient is 1 year old.

The recently developed thrombin injection has been an excellent minimally invasive modality for treating pseudoaneurysms. Most pseudoaneurysms are iatrogenic and are complications of arterial injections; the next most frequent cause is infection, followed by external trauma. Pseudoaneurysms are generally symptomatic and any pain is due to compression of adjacent structures. The most common site of occurrence is the femoral artery, specifically at the junction of the common and deep femoral arteries. These lesions are best evaluated using duplex ultrasonography, which defines their morphology, location, and size.

Epigastric hernias are frequently multiple, which must be considered when deciding how to treat affected patients. Epigastric hernias occur almost exclusively in males and adults. Because the defects are tiny, pain is caused by incarceration of preperitoneal fat. These hernias can be primarily repaired without using mesh.

Operation is indicated after 4 to 6 units of blood have been transfused, as long as the patient remains stable. Hemodynamic instability is an indication for operation, as is the failure of endoscopic therapy to stop bleeding. Patients who bleed but have no prior symptoms have a 30% chance of hemorrhage recurring, which is again likely to begin suddenly, with no previous symptoms or early warning signs; this scenario carries a 20% mortality rate. Patients with ischemic heart disease cannot tolerate any decrease in blood pressure; consequently, early operation is indicated in this group of patients.

American Board of Surgery Recertification Examination

	Aseptic technique for performing central venous catheter exchange... (Jan. 2008)

	The technique described appears to be what was taught to me 20 years ago at the University of Wisconsin at Madison. I would be surprised if Dr. Dennis Maki didn't publish some information as to infection rates. If not, he may have unpublished data the author may be interested in. I do cringe at the picture of feeding the guidewire into the catheter without some grip on the catheter, with the cut end so close to the skin, even though the text states to hold the catheter. This is a good way to embolize the catheter, maybe not as easily with an internal jugular venous access, but a subclavian slides more easily.

As stated in the abstract, I am not aware of any published reports that mention the technique described in this article. However, I realize that other institutions may have used the same or similar techniques when guidewire exchange is necessary. I am well aware of Dr. Maki's numerous contributions to the literature regarding catheter-related bloodstream infections. As for the reader's concerns regardingFigure 4, which demonstrates a guidewire being fed into the catheter, the assistant's hand was removed only to allow the picture to be taken. The guidewire is never advanced into the catheter unless it is held securely. Although catheter embolization is theoretically possible with this technique, I have not experienced any catheter movement when advancing the wire.

	I was jealous to find that Dr. Cunningham's technique of cutting the central line's ports is nearly the same as what I developed during my quest to find the cleanest way to exchange catheters. I wish to recommend one modification, which requires only one operator and, I feel, is cleaner. I recommend asking an assistant to hold the ports in the air as the operator preps the area and cuts the stitches. This way, you can place the sterile field over the ports, the assistant can let them go and thus exclude them completely from the field. The rest is just as Dr. Cunningham described.

 warn others of a potentially disastrous situation that can occur if this technique is used on the wrong catheter. In my enthusiasm for the technique, I once tried it during the exchange of a double-lumen 9F introducer (commonly referred to as a "Cordis") central venous catheter. After cutting it, I was about to insert my wire when I noticed something in the lumen, which I was fortunately able to clamp and retrieve. Cutting these catheters leaves the central lumen completely free-floating, and it could easily migrate into the patient's venous system, particularly if you push the guidewire. Do not try to cut a double lumen introducer or you risk embolizing the innermost tube!

	(See: Galli S, et al. Accidental migration of ASH-split catheter during central venous catheter replacement: retrieval using an interventional radiology approach. 

	 have been using Dr. Cunningham's technique for changing central lines since 1984. Dr. Stanley Dudrick taught it to me when I did a general surgery and nutrition fellowship with him that year. I always use a hemostat on the catheter to lessen the risk of air or catheter embolism. It is a nice technique and has worked well for my patients over the years.

Aseptic technique for performing central venous catheter exchange.

, General Surgery Chief Resident, Synergy Medical Education Alliance/St. Matthew's University, Saginaw, MI; and 

, General Surgery Program Director, Synergy Medical Education Alliance, Associate Professor of General Surgery, Michigan State University, Saginaw, MI

	A 62-year-old woman presented to the hospital reporting a 1-week history of nausea, mild abdominal pain, constipation, and emesis, which was bilious and nonbloody. Her abdominal pain, primarily in the epigastric and right upper quadrant, was dull and nonradiating. She had an episode of diarrhea 7 days earlier, followed by constipation, and had not passed flatus for 1 to 2 days. The patient's medical history was significant for diabetes, which was controlled through diet.

	All the patient's vital signs were within normal limits. Her abdomen was soft and mildly distended, with tenderness in the epigastric area and the right upper and lower quadrants. Palpation elicited no rebound or guarding and was negative for Murphy's sign. No fluid thrill was noted and bowel sounds were hypoactive on auscultation. No hernias were appreciated, and she was anicteric. Laboratory tests revealed the following: white blood cell count, 16,100/mm

; neutrophils, 0.851; hemoglobin, 15 g/dL; total bilirubin, 22.23 μmol/L; aspartate aminotransferase, 20 U/L; alkaline phosphatase, 37 U/L; amylase, 45; and lipase 51 U/L.

	An abdominal radiograph and abdominal and pelvic computed tomography scans were obtained 

	What is causing this patient's intestinal obstruction?

		The abdominal radiograph shows dilated loops of small bowel, air fluid levels, and a large amount of stool in the colon. The computed tomography (CT) scans demonstrate a thickened structure in the gallbladder fossa containing air and contrast; other findings include pneumobilia, a cholecystoduodenal fistula, and a sizeable gallstone in the distal jejunum, with dilated loops of bowel proximal to this point. Our diagnosis was gallstone ileus resulting in jejunal obstruction.

		During open enterolithotomy, a 4.5 x 3.5 x 2.0 cm gallstone was removed from the jejunum (

). The enterotomy was repaired transversely, and the gallbladder, biliary tract, and cholecystoduodenal fistula were left undisturbed. The patient suffered postoperative ileus, requiring 3 days of nasogastric decompression. She was discharged on postoperative day 6 and has had no further symptoms.

—Intraoperative photograph of the open enterolithotomy showing a large gallstone in the distal jejunum (A) and a pathology image of the gallstone, which measured 4.5 x 3.5 x 2 cm (inset).

		Gallstone ileus is a rare cause of intestinal obstruction and is most common in women aged 74 to 80 years.

 It accounts for less than 4% of all bowel obstructions and more than 25% of nonstrangulated bowel obstructions in patients older than 65 years, and its mortality rate is 15% to 18%.

 Patients often present with abdominal pain and vomiting, but no signs or symptoms specific to gallbladder or intestinal disease. Less than 25% of patients noted biliary colic in the year prior to diagnosis.

		Obstruction occurs when a gallstone 2.5 cm or larger passes through a cholecystoenteric fistula into the intestinal lumen. Fistulas form during repeated attacks of cholecystitis, and the most common are cholecystoduodenal, followed by cholecystocolonic, cholecystogastric, and choledochoduodenal. More than 80% of gallstones that migrate to the bowel are excreted,

 but a gallstone can cause obstruction anywhere along the gastrointestinal tract from the duodenum to the colon. The most common site of intestinal obstruction is the distal ileum near the ileocecal valve, which is the narrowest section of the small bowel.

		When gallstone ileus is suspected, abdominal radiographs should be examined for Rigler's triad of pneumobilia, intestinal obstruction, and aberrantly located gallstones, although only 40% of cases demonstrate such findings.

 CT scanning has increased the rate of preoperative diagnosis and should be used when abdominal radiographs or ultrasonography findings are inconclusive. Only 13% to 48% cases of gallstone ileus are diagnosed preoperatively,

 and diagnosis and treatment are frequently delayed, with an average of 2 to 5 days from admission to surgery.

		Gallstone ileus is a surgical emergency. Enterolithotomy, with a mortality rate of 11.7%, is the gold standard of treatment. Surgical-site infections are the most common cause of morbidity. Some argue that laparoscopic enterolithotomy reduces this risk and should be considered, depending on the patient's situation and the surgeon's experience performing the procedure.

		Management of the cholecystoenteric fistula is controversial. Because patients with gallstone ileus are usually elderly and high-risk with concomitant medical disease, the literature generally supports enterolithotomy alone, which is associated with shorter surgical times and a lower mortality rate when compared with one- and two-stage procedures. These operations are far more complex, and most authors agree they should be reserved for low-risk patients, when practical, or in cases of gallbladder necrosis and empyema.

The authors have no relationship with any commercial entity that might represent a conflict of interest with the content of this article and attest that the data meet the requirements for informed consent and for the Institutional Review Boards.

			Reimann AJ, Yeh BM, Breiman RS, et al. Atypical cases of gallstone ileus evaluated with multidetector computed tomography. 

			G?rleyik G, G?rleyik E. Gallstone ileus: demographic and clinical criteria supporting preoperative diagnosis. 

			Wig JD, Suri S. A good computed tomography in gallstone ileus. 

			Anagnostopoulos GK, Sakorafas G, Kolettis T, et al. A case of gallstone ileus with an unusual impaction site and spontaneous evacuation. 

			Lobo DN, Jobling JC, Balfour TW. Gallstone ileus: diagnostic pitfalls and therapeutic successes. 

			Shenoy VN, Limbekar S, Long PB, et al. Relief of small bowel obstruction following colonoscopy in a case of gallstone ileus. 

			Ferraina P, Gancedo MC, Elli F, et al. Video-assisted laparoscopic enterolithotomy: new technique in the surgical management of gallstone ileus. 

Darin F. Doumite, Medical Student IV, Synergy Medical Alliance/St. Matthew's University, Saginaw, MI; Brian Beeman, MD, Synergy Medical Alliance/St. Matthew's University, Saginaw, MI; and Dennis Boysen, MD, Synergy Medical Education Alliance and Michigan State University, Saginaw, MI

What is causing this patient's intestinal obstruction?

: Hyperkalemia is characterized by excessive potassium in the blood. Sodium polystyrene sulfonate (SPS), also known as Kayexalate and Kionex, is a water-soluble resin used to treat patients with this condition. When an SPS solution is ingested, it binds to potassium, and the SPS-potassium compound is then excreted. SPS is sometimes mixed with sorbitol, a polyalcohol sugar, to induce faster passage through the digestive system.

: Studies suggest that combining SPS with sorbitol to treat hyperkalemia can cause gastrointestinal complications in uremic patients. The authors report the case of a 55-year-old man admitted to the hospital because of scrotal cellulitis. The patient had undergone a kidney transplant a decade earlier and continued to suffer from chronic renal failure. He received a solution of SPS in sorbitol for 2 days and consequently developed pneumatosis intestinalis and a perforated colon. He underwent total colectomy with end ileostomy but died 7 days postoperatively. A pathology examination of the colectomy specimen found extensive mucosal necrosis and evidence of SPS-induced ischemia.

: The literature reports that anywhere from 36% to 80% of uremic patients treated with SPS-sorbitol for hyperkalemia die from complications. In 2003, the Food and Drug Administration added a precaution to the labels of SPS drugs (Kayexalate, Kionex), advising that SPS-sorbitol had been "implicated in cases of colonic necrosis" and therefore should not be administered concomitantly. Clinicians who administer SPS-sorbitol to hyperkalemic patients must remain vigilant for any signs or symptoms of intestinal problems. Aggressive evaluation and management are imperative to prevent significant morbidity and death.

	Sodium polystyrene sulfonate (SPS), sold under the brand names Kayexalate and Kionex, is a potassium-binding resin that has been in use in the United States since 1975.

 It is used in treating patients who have hyper-kalemia, a sometimes life-threatening condition marked by an excessive level of potassium in the blood. SPS works by exchanging sodium for gastric hydrogen in the stomach. As the resin passes into the intestines, the hydrogen ions are exchanged for potassium. The resin-potassium compound is then excreted into the stool. SPS initially was administered in a water solution, but the resin tended to pass through the digestive system slowly, causing be-zoars, fecal impactions, and obstructions. To prevent these problems, the SPS was mixed with sorbitol, a polyalcohol sugar that serves as a hypertonic agent. The small intestine absorbs sorbitol poorly, which can result in osmotic diarrhea.

Bacterial flora process the sorbitol in the colon, where it is absorbed and frequently causes colonic complications.

 We report the case of a uremic patient who developed hyperkalemia and was administered SPS in sorbitol. The patient developed ischemic colitis and died.

	A 55-year-old man was admitted to the hospital due to scrotal cellulitis. His medical history included diabetes and chronic renal failure, for which he had received a cadaveric renal transplant 10 years earlier. He was started on parenteral antibiotic therapy, adjusted to account for his renal failure. Despite treatment, his renal function worsened, and he developed mild hy-perkalemia. The patient received three doses of an oral SPS-sorbitol solution over 2 days to correct his hyperkalemia, but he showed no improvement and was started on hemodialysis. He developed diarrhea and became febrile (40°C). Blood and stool cultures were negative for pathogens. He described feeling diffuse abdominal pain and distention. During a physical examination, no bowel sounds were heard on auscultation.

	Computed tomography (CT) scans of the patient's abdomen showed pneumatosis intestinalis of the ascending and descending colon, perforation of the ascending colon, and free air 

An exploratory laparotomy confirmed the CT findings, and total colectomy with end ileostomy was performed. No evidence of colonic necrosis was observed.

	Pathology examination of the colectomy specimen noted extensive mucosal necrosis with ischemic features and luminal SPS crystals, consistent with SPS-induced ischemia 

Thomas J. Douglas, MD; Richard P. Sharpe, MD; and Paul A. Lucha, DO, Naval Medical Center, Portsmouth, VA

April 2008

Idiopathic pneumoperitoneum after blunt chest trauma

'Difficult' patients

Why America?

American Board of Surgery Recertification Examination

Aseptic technique for performing central venous catheter exchange.

What is causing this patient's intestinal obstruction?

Is sodium polystyrene sulfonate (Kayexalate, Kionex) in sorbitol deadly to uremic patients?

Presacral lymphangioma: A rare cystic tumor

Epithelioid hemangioendothelioma of the peritoneum

Teatro Anatomico