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The balloon tamponades liver hemorrhage. The catheter is brought out through the abdominal wall, deflated, and removed 24�48 hours later. Liver packing with planned reoperation for definitive treatment of injuries in patients who have hypothermia, acidosis, and coagulopathies is a life-saving maneuver damage control laparotomy.

The abdominal compartment syndrome is a potentially lethal complication of perihepatic packing or large volume resuscitation. It may occur when intraabdominal pressure exceeds 20 cm H2O. Intraabdominal pressure increases because of bowel and liver edema secondary to ischemia and reperfusion injury or continued hemorrhage into the abdominal cavity.

As pressure increases beyond 20 cm H2O, venous return, cardiac output, and urine output decrease, but ventilatory pressures increase. Patients must return promptly to the operating room for decompression of the abdomen.

A manometer attached to the Foley catheter is useful in following intraabdominal pressure. Complications include bleeding, biliary leaks or fistulae, abdominal compartment syndrome, and infection.

Bilomas i. Biliopleural fistula, a communication between the biliary system and pleural cavity, persists because of the relative negative pressure in the thorax and may result in a bile empyema. Bilhemia results from an intrahepatic fistula between the bile ducts and hepatic veins, resulting in severely elevated bilirubinemia.

Hemobilia occurs from the rupture of an arterial pseudoaneurysm into the biliary system, resulting in upper gastrointestinal hemorrhage. Leak rates are higher for those who undergo operations or angioembolization. Perihepatic fluid collections identified by US suggest a leak; however, they are more accurately identified by hepatobiliary iminodiacetic acid scan or endoscopic retrograde cholangiopancreatography ERCP.

ERCP is usually quite useful in diagnosing and treating leaks. Biliary stenting with or without sphincterotomy and percutaneous drainage of bilomas frequently allows spontaneous resolution of bile duct injuries. Extensive injuries require hepaticojejunostomy or reconstruction.

Angioembolization is an important adjunct. Nonoperative management of blunt hepatic trauma is the treatment of choice for hemodynamically stable patients.

Surgical anatomy of the hepatic arteries in cases. Trauma surgeons practice what they preach: the NTDB story on solid organ injury management. Nomenclature of hepatic anatomy and resections: a review of the Brisbane system. J Hepatobiliary Pancreat Surg. Nonoperative management of adult blunt hepatic trauma: the exception or the rule.

Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Organ injury scaling. Surg Clin North Am. Nonoperative management of blunt hepatic trauma: a systematic review. Balloon tamponade for bilobar transfixing hepatic gunshot wounds. A year experience of complex liver trauma.

Br J Surg. High success with nonoperative management of blunt hepatic trauma: the liver is a sturdy organ. Arch Surg. Blunt liver injury: from non-operative management to liver transplantation. Diagnosis and management of bile leaks after blunt liver injury. Evans, MD, Eric M. Campion, MD, Ernest E. In fetal development, the spleen serves as a major site of hematopoiesis. Later in life the spleen produces immunoglobulin M IgM , properdin, and tuftsin, important factors in immunologic function.

The spleen also acts as a filter, allowing resident macrophages to remove abnormal red blood cells, cellular debris, and encapsulated and poorly opsonized bacteria. Mechanisms associated with splenic injury include direct blunt force, deceleration, and compression to the left torso.

Splenic injuries should be considered after any significant motor vehicle accident or fall�lower rib fractures, left-side-only rib fractures, and high-energy transfer increase the probability of splenic injury. The most common sign is pain in the left upper quadrant produced by stretching of the splenic capsule.

Peritoneal irritation rebound tenderness is caused by extravasated blood. Vital signs vary depending on the associated blood loss and are not specific for injuries to the spleen. On the other hand, patients with a significant splenic injury may exhibit no signs or symptoms at all. A common scenario is to have a shoulder radiograph performed after a fall when the pain is actually from a ruptured spleen.

Focused assessment with sonography for trauma FAST is routinely performed in the emergency department and can rapidly identify as little as mL of fluid or blood, although this finding is nonspecific for splenic injury. When FAST is equivocal, diagnostic peritoneal lavage is an accurate and sensitive measure of intraabdominal bleeding but is also nonspecific.

Computed tomography CT scanning is the gold standard diagnostic test because of its ability to identify splenic injuries with a high sensitivity, define the magnitude of injury, and identify concomitant injuries. Splenic injuries are classified based on the American Association for the Surgery of Trauma splenic injury scale Table Operative versus nonoperative management NOM is governed by the hemodynamic status of the patient and concomitant injures.

NOM is influenced by the CT grade of splenic injury. Hemodynamically unstable patients should undergo operative management of splenic injuries. SAE has increased the rate of successful NOM and should be considered in high-risk patients, including grade IV�V injuries as well as all splenic injuries with contrast extravasation on CT scan.

ERCP is the most accurate method of identifying an injury to the pancreatic duct. Magnetic resonance cholangiopancreatography MRCP is a useful modality to identify pancreatic injury with ductal involvement, and has an added advantage of evaluating the duct distal to a transection; however, therapeutic maneuvers are not possible with MRCP. Elevated serum amylase concentrations are nonspecific for pancreatic injury and can be normal initially in a high proportion of patients.

The majority of pancreatic injuries can be treated with the placement of closed suction drains at the time of initial laparotomy. In situations of more severe trauma, the integrity of the pancreatic duct must be investigated through direct inspection or pancreatography.

Injuries involving the duct portion of the pancreatic duct are managed with a distal pancreatectomy and drain placement.

If the patient is in extremis, a splenectomy should be performed during the distal pancreatectomy. However, if a patient is hemodynamically stable, a spleen preserving distal pancreatectomy is preferred.

Injuries involving the pancreatic duct proximal to the mesenteric vessels may require a significant resection such as a pancreaticoduodenectomy. Extensive resections such as these are generally performed following a damage control situation at the follow-up operation. Exsanguination, as with most traumatic injuries, is the most common cause of early death, prompting the use of damage control.

For patients who survive their initial operation, the two most common complications are pancreatic fistulas and intraabdominal abscesses.

Other late problems include pancreatitis, pancreatic pseudocyst, and pancreatic hemorrhage. Careful attention to the injury pattern and location of injury in relation to the mesenteric vessel should lead to the correct surgical operation.

Resection of the pancreas distal to the mesenteric vessels should allow enough pancreas to remain for sufficient exocrine and endocrine function. Most patients who die after sustaining injuries to the pancreas do so as a result of late complications and not from the pancreatic injury itself. CT evaluation of a hemodynamically stable patient sustaining blunt trauma is the diagnostic modality of choice. Specific direct signs of bowel injury, pneumoperitoneum, or oral contrast extravasation indicate injury to the hollow viscus and mandate operative exploration.

Indirect evidence of a duodenal injury includes periduodenal fluid or hematoma, focal pneumatosis, adjacent vascular or organ injury, and fatty stranding in the retroperitoneum, which are nonspecific findings. Isolated periduodenal fluid or hematoma does not mandate an operative exploration. A safe management algorithm should include observation with serial examinations and an interval CT scan at 24 hours.

In , E. Theodor Kocher described a maneuver to visualize and repair injuries to the duodenum, distal common bile duct, and pancreatic head during exploratory surgery.

The avascular lateral peritoneal attachments to the duodenum are incised sharply, and the duodenum is elevated and reflected medially from the retroperitoneum to the border of the inferior vena cava. This allows for inspection and palpation of the posterior surface of the duodenum and head of the pancreas.

The first portion of the duodenum begins at the pylorus, making it an intraperitoneal structure. It then migrates into the retroperitoneum as it passes by the gallbladder.

The second portion descends 7�8 cm through the retroperitoneum anterior to the vena cava. The medial border of the duodenum is adherent to the head of the pancreas where the common bile and pancreatic ducts enter; it shares a common blood supply with the head of the pancreas through the pancreaticoduodenal arcades.

The third portion of the duodenum turns horizontally through the retroperitoneum contacting the uncinate process along its superior border and passing behind the root of the mesentery. The fourth portion continues horizontally, ascending slightly and crossing the spine anterior to the aorta, where it is fixed to the suspensory ligament of Treitz at the duodenojejunal flexure, medial to the inferior mesenteric vein. An organ injury scale has been adopted that allows for standardized descriptions of duodenal injuries, which extend from grade I less severe to grade V most severe.

The grading of duodenal injuries assists surgeons in selecting the appropriate surgical procedure for the repair or reconstruction of these frequently complex injuries see Table If tension on the suture line is anticipated following resection of devitalized tissue, adjunctive techniques such as Roux-en-Y duodenojejunostomy or pyloric exclusion in conjunction with a gastric drainage procedure are more appropriate. Injuries involving the distal common bile duct and pancreatic head may warrant a pancreaticoduodenectomy after damage control procedure.

Consideration should be given to establishing enteral access, especially in all complex repairs. Most injuries can be managed with simple primary repair. Extensive resections should be delayed in hemodynamically unstable patients via damage control procedures.

Predictors of morbidity and mortality in patients with duodenal injuries. Am Surg. Predictors of morbidity after traumatic pancreatic injury. Recent trends in the management of combined pancreatoduodenal injuries. Organ injury scaling II: pancreas, duodenum, small bowel, colon, and rectum.

Imaging of pancreatic trauma. Br J Radiol. The managing of pancreatic trauma in the modern era. Serum amylase level on admission in the diagnosis of blunt injury to the pancreas: its significance and limitations. Role of duodenography in the diagnosis of blunt duodenal injuries. A prospective study of post-traumatic biliary and pancreatic fistuli. The role of expectant management. Safety of repair for severe duodenal injuries.

World J Surg. Long-term outcome after nonoperative management of complete traumatic pancreatic transection in children. J Pediatr Surg. Management of splenic and pancreatic trauma.

J Visc Surg. Distal pancreatectomy for trauma: a multicenter experience. Morbidity and mortality after distal pancreatectomy for trauma: a critical appraisal of consecutive patients undergoing resection at a Level 1 Trauma Centre. Indirect signs of blunt duodenal injury on computed tomography: is non-operative management safe? Isolated blunt duodenal trauma: simple repair, low mortality. Imaging of pancreatic and duodenal trauma. Rad Clin Nor Am. Blunt colonic trauma is rare and usually results from seat belts during motor vehicle crashes.

They are usually diagnosed during laparotomy for penetrating trauma. For patients in whom the need for laparotomy has not been established, a rectal examination may show blood in the stool, which suggests a left-sided or rectal injury. Elevated white blood cell counts or enzyme levels amylase, alkaline phosphatase may reflect a bowel injury.

While no longer commonly performed, fecal material in diagnostic peritoneal lavage is highly suggestive of a bowel injury. Imaging findings that are concerning for a colonic injury include free air, extravasation of contrast, retroperitoneal gas, or fluid adjacent to the colon. All significant injuries are generally clinically manifest within 18 hours of injury. Flexor tendon lacerations are not an emergency, and should therefore not be repaired in the ED. If a hand surgeon is unavailable, the wound is copiously irrigated and skin sutured closed.

Prophylactic antibiotics need to be administered and the hand splinted in a metacarpophalangeal MP and IP joint flexing dorsal splint. This injury should be treated within the first 10 days. Delays in treatment can preclude the ability to perform primary tendon repairs. Open fractures proximal to the MCP joint should be cleaned and dressed in the ED, but not probed or cultured.

A first-generation cephalosporin, such as Ancef, is administered and tetanus immunization updated. Open fractures meeting the criteria of the Gustilo and Anderson classification should receive additional penicillin and an aminoglycoside, such as Gentamicin. A saline-soaked dressing is applied over the wound, and the hand is splinted in a functional position using a bulky dressing. Urgent irrigation and debridement in the OR is indicated followed by fracture stabilization and wound closure.

The extremity should be immobilized and elevated, and antibiotics should be administered. Serial examinations should be used to assess for improvement. The patient should be referred for possible surgical drainage especially if concern for abscess or deeper infection exists.

After wound cleansing, radiographs are obtained to rule out foreign bodies e. Wounds are left open and antibiotics are started. Keep a high level of suspicion for infection in all puncture bites that inoculate deep structures and have no drainage e. All wounds are rechecked at 24 and 48 hours. If evidence of infection is present, parenteral antibiotics should be instituted and the patient referred for possible surgical drainage. In human bites, the most common microorganisms are Staphylococcus aureus, alpha hemolytic Streptococcus, and Eikenella corrodens.

This often inoculates the MCP joint with anaerobic Streptococci. The resulting traumatic arthrotomy can be difficult to identify, especially when examining the hand flat on the examination table and not in the initial clenched position. These injuries require irrigation and debridement in the OR. Early infections can be treated with antibiotics and soaks. More established infections require drainage under digital block.

Drainage through a longitudinal incision is the recommended treatment. Other incisions may destabilize the fingertip pulp from the underlying distal phalanx. Infections in these locations can be missed. Despite their innocuous appearance, injection injuries may cause profound destruction of hand structures. Any such injury requires immediate hospitalization with emergent irrigation and debridement. Multiple, second look debridements may be required.

The prognosis is guarded when oil-based paint or industrial solvents are involved. Latex and water-based paints cause less tissue damage. Edema and infection lead to increased scarring and restricted function. Prolonged immobilization in a poor position also impairs function. Failure to obtain radiographs may lead to a missed or delayed diagnosis of an injury. Patients need to be treated according to the advanced trauma life support protocol. In addition to cardiopulmonary stabilization, tetanus immunization and prophylactic antibiotics are administered.

Broad-spectrum antibiotics should be given in heavily contaminated wounds or in diabetic or immunocompromised patients. Photo documentation of soft tissue injuries is helpful. While tests are pending, a replantation center is contacted for transfer. Prolonged ischemia of the amputated part risks the possible success of replantation attempt. Once the patient is accepted, expedited transfer is mandatory, which may include airlifting.

Digital replantation is usually possible up to 24 hours. The larger the amputate size including the amount of severed muscle forearm and arm level injuries the shorter the ischemia tolerance.

Major amputations proximal to the palmar arch are usually not replantable beyond 6 hours of cold ischemia time. The amputated part is wrapped in saline-soaked gauze and sealed in a plastic bag. Direct contact with ice must be avoided to prevent freezing. Hypotonic and hypertonic solution should not be used to prevent osmotic damage to the part. Acute compression of the median nerve in the carpal tunnel is a condition associated with trauma to the hand, wrist, or forearm.

Examples are distal radius fractures or a perilunate dislocation. This clinical diagnosis presents with worsening wrist pain and sensory changes in the median nerve distribution, which typically include paresthesias in the volar thumb, index, middle, and half of the ring finger. The hallmark of acute carpal tunnel syndrome is progressive neurologic changes in the median nerve distribution. Emergent decompression of median nerve by releasing the transverse carpal ligament.

No suture closure of bite wounds in the ER. The emergent evaluation and treatment of hand injuries. Emerg Med Clin North Am. Philadelphia: Elsevier; Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: retrospective and prospective analyses.

J Bone Joint Surg Am. Hand injuries in agricultural accidents. J Hand Surg Br. Open extensor tendon injuries. J Hand Surg Am. Hand infections. Hand Clin. Human and other mammalian bite injuries of the hand: evaluation and management. J Am Acad Orthop Surg. Acute carpal tunnel syndrome.

Orthop Clin North Am. Controversies in the treatment of fingertip amputations: conservative versus surgical reconstruction. Clin Orthop Relat Res. J Hand Ther. A prospective, randomized, controlled trial of 2-octylcyanoacrylate versus suture repair for nail bed injuries.

Karel D. Capek, MD, David N. Eighty percent of burn-related injuries occur in the home, mostly in low-income, multifamily dwellings.

The incidence of burn injuries and deaths in the United States is substantially higher than that of the rest of the industrialized world. The male-to-female ratio for burn injuries is roughly Alcohol abuse and illicit drug activity increase the risk of burn injury. The overall mortality risk of burns is 7. Survivors currently reported to Systemic infection or sepsis remains the dominant precipitant of organ failure and death; this points to a burn injury-related immune dysfunction or failure.

The injury site may be divided into three zones by standard light microscopy: An inner zone of necrosis, a middle zone of stasis, and an outer zone of hyperemia. In the zone of necrosis, proteins are denatured; all microvascular and macrovascular structure and function are destroyed. Surrounding this central zone is a zone of stasis.

Here, cellular morphology is intact, but cells are swollen with microstructural changes with extravasation of leukocytes and red blood cells into the interstitial space, increased interstitial fluid, and capillary stasis. A third zone of hyperemia then transitions into the adjacent normal tissues where no abnormalities are seen.

Other physical trauma is frequently associated with explosions or merely the attempts to escape the fire. Awareness of associated trauma justifies the importance of a careful advanced trauma life support trauma evaluation. Depending on mechanism, eye injuries, tympanic membrane rupture explosions , and pneumothorax may accompany burn injury. Thus, burn injury is accompanied by interrelated changes in volume status, vascular tone, and cardiac pump function.

This includes alterations in heat exchange via all four mechanisms of heat dissipation: radiant body surface blood flow , convective hair position , evaporative sweating and wound exudate , and conductive determined by the ambient temperature and temperature of objects in contact with the patient.

First, do no harm. No ice, butter, dry ice, or any other substance should be applied to the wound after extinguishing the fire. Polyps with margins 35 with weight-related comorbidities and the ability to understand and comply with the perioperative routine. The latter is extremely important because the patient must relearn how to eat with his or her new anatomy. This operation is not without risk and has significant health and social consequences�imagine going out to dinner when you can eat only 10 teaspoons.

Leak of the gastrojejunal anastomosis is the most feared complication, though it is second to pulmonary embolism as a cause of death in most series. The mortality rate is should prompt concern for a leak. Some surgeons order routine contrast studies in all patients. Long-term mortality after gastric bypass surgery. N Engl J Med.

Laparoscopic versus open gastric bypass for morbid obesity: a multicenter, prospective, risk-adjusted analysis from the National Surgical Quality Improvement Program. Metabolic syndrome: yet another co-morbidity gastric bypass helps cure. Surg Obes Relat Dis. Laparoscopic Roux-en-Y gastric bypass: surgical technique and perioperative care. The prevalence of hyperparathyroidism is Seventy-four percent of all cases are in women, and the risk increases with age. Primary HPT occurs in 1 in women and in 1 in men older than age Painful bones, renal stones, abdominal groans, psychic moans, and fatigue overtones.

HPT is the most common cause of hypercalcemia among outpatients and the second most common cause in the hospital setting. The most common cause of hypercalcemia in hospitalized patients is malignancy.

The diagnosis of primary HPT is confirmed with an elevated serum calcium level, elevated parathyroid hormone PTH , and the absence of low hour urine calcium. An elevated serum calcium should be assessed at least twice and must be associated with elevation of intact PTH. Patients with elevated alkaline phosphatase associated with increased blood urea nitrogen and creatinine are at increased risk of hungry bone syndrome after parathyroidectomy.

A normal parathyroid response to elevated serum calcium is decreased PTH secretion. When serum calcium is high, the PTH level should be at the low end of normal. A PTH level at the high end of normal in the setting of hypercalcemia is inappropriately elevated and consistent with primary HPT. One should rule out FHH by testing hour urine calcium.

Occasionally, patients will be identified with an elevated PTH level and a normal serum calcium. This entity exists on the diagnostic spectrum of PHPT, and calcium is typically at the upper limits of the normal range.

The majority of these patients will have an elevated ionized calcium. Patients with untreated primary HPT have increased death rates caused by hypercalcemia-related cardiovascular disease. Patients also have improvements in abnormal quality-of-life scores after operative success, and the costs of surgery are equivalent to that of medical follow-up at 5 years. The American Joint Committee on Cancer staging for cutaneous squamous cell carcinoma 8th ed. Modality of treatment depends on the tumor subtype, location, and presence of high-risk features.

Most tumors are treated with wide local excision or Mohs micrographic surgery. Topical immunomodulators, topical chemotherapeutic agents, and electrodessication and curettage are suitable for some low-risk NMSCs.

Each treatment option will be discussed in more detail in the following questions. Occasionally, radiation therapy is considered for patients who are poor surgical candidates or as adjuvant therapy for invasive or metastatic disease. Some large SCCs require a 1 cm margin. After the tissue is removed, a map is created with corresponding ink marking of the tissue edges for orientation. The tissue is frozen and placed on slides for hematoxylin and eosin staining and subsequent evaluation by the Mohs surgeon.

If the tumor remains at any margin, another layer of tissue is removed in that specific location and again evaluated microscopically for evidence of residual tumor. This process is repeated until the entire tumor is removed.

Mohs surgery can be considered for any tumor with a contiguous growth pattern. The Appropriate Use Criteria AUC for Mohs surgery is a set of guidelines created by a joint committee in to help prevent the overuse of Mohs surgery, while appropriately triaging those patients who would benefit from this technique. Immunosuppressed patients with high-risk tumors could also be considered for sentinel lymph node biopsy. Which gene is mutated in this condition?

Gorlin syndrome basal cell nevus syndrome is an autosomal dominant condition characterized by a mutation in the PTCH1 gene. PTCH1 is a tumor suppressor in the Hedgehog signaling pathway, and loss of this gene leads to tumor proliferation. These patients develop BCCs starting in adolescence. They also have palmar pits, frontal bossing, medulloblastomas, odontogenic keratocysts of the jaw, and abnormalities of the vertebrae and ribs. Vismodegib and Sonidegib are targeted molecular inhibitors of the Hedgehog signaling pathway.

This medication carries significant side effects of muscle cramps, alopecia, and dysgeusia. It is teratogenic and so should not be used in women of childbearing potential. The precursor lesion to cutaneous SCC is the actinic keratosis. Actinic keratoses are rough pink papules in sun-exposed areas that represent in-situ dysplasias. Field treatment to the most severely affected areas should be considered in patients with numerous actinic keratoses.

Options include cryotherapy, topical 5-fluorouracil, imiquimod, ingenol mebutate, or photodynamic therapy. These treatments are similar in efficacy for the treatment of actinic keratoses. What are the side effects? Acitretin is a systemic retinoid that can be considered for patients with numerous SCCs. It decreases the development of new primary lesions and is commonly used in solid organ transplant patients with numerous SCCs.

The major side effects include teratogenicity, transaminitis, hyperlipidemia, and dryness of the eyes, lips, mouth, and skin. How should they be counseled? Patients should have a full-body skin examination by a dermatologist every 6 months for the first 2 years after an NMSC.

If no additional skin cancers are found during that period, exams can then be spaced annually. Strict photoprotection will decrease the development of new primary NMSC, and the patient should be counseled accordingly. The AUC for Mohs surgery is an excellent guide of when to place a referral. These patients should be referred to a dermatologist for regular skin examinations. Incidence estimate of nonmelanoma skin cancer keratinocyte carcinomas in the US Population, JAMA Dermatol.

American Cancer Society, Surveillance Research, Accessed March Fast Facts: Skin Cancer. Health Press Limited; Clinics Sao Paulo. A pilot study to evaluate the treatment of basal cell carcinoma with 5-fluorouracil using phosphatidyl choline as a transepidermal carrier. Dermatol Surg. Topical treatment strategies for non-melanoma skin cancer and precursor lesions.

Semin Cutan Med Surg. Topical imiquimod or fluorouracil therapy for basal and squamous cell carcinoma: a systematic review. Arch Dermatol. Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol. Cutaneous squamous-cell carcinoma. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip: implications for treatment modality selection.

High-risk cutaneous squamous cell carcinoma and the emerging role of sentinel lymph node biopsy: a literature review. Cutaneous squamous cell carcinoma of the head and neck. New York: Springer; � Epidermal nevi, neoplasms, and cysts. Philadelphia: Elsevier; � A new American Joint Committee on Cancer staging system for cutaneous squamous cell carcinoma: creation and rationale for inclusion of tumor T characteristics.

The paired parotid glands are the largest of the three major salivary glands. The parotid gland is triangular in shape bounded superiorly by the zygomatic arch; posteriorly by the external auditory canal; inferiorly by the styloid process, the styloid muscle, and the jugular and internal carotid vessels; and anteriorly by the masseter muscle. The tail of the parotid gland may extend inferior-posterior to the level of the sternocleidomastoid muscle and mastoid process.

Its main histologic feature consists of clusters of acinar cells that are mainly serous secreting. The parotid salivary gland units consist of the acinar cells of the parotid gland and a transport system. The transport system consists of the following: the intercalated ducts, the striated ducts, and the excretory ducts. Contractile myoepithelial cells surrounding both the acinous cell units and the intercalated ducts force the watery secretions through the duct system into the oral cavity.

The facial nerve divides the parotid gland into a superficial and deep lobe. The facial nerve enters the temporal bone at the anterior superior portion of the internal auditory canal. The nerve then travels through the mastoid bone in the fallopian canal exiting the skull base at the stylomastoid foramen. The nerve lies lateral to the styloid process and posterior belly of the digastric muscle and medial to the mastoid tip. As the nerve exits the stylomastoid foramen, it immediately gives off three motor branches: one to the stylohyoid muscle, one to the posterior belly of the digastric muscle, and the third to the three postauricular muscles of the pinna.

The nerve then proceeds anteriorly for a short distance and at the pes anserinus divides into two major divisions�the temporofacial and cervicofacial divisions. After dividing, the nerve will then turn laterally to enter the posterior aspect of the parotid gland. The temporofacial division subsequently divides into the temporal, zygomatic, and buccal branches.

The cervicofacial division divides into the marginal mandibular and cervical branches. The deep parotid lobe lies between the temporofacial and cervicofacial divisions.

There are numerous variations in the division of the nerve, and careful identification of each division and branch must occur to avoid injury to the nerve. The temporal and marginal mandibular branches of the facial nerve are at major risk of injury because of their small size and lack of anastomotic connections. Careful identification and dissection is extremely important. There are currently two theories of tumor development based on the salivary gland unit.

The intercalated duct reserve cells give rise to the pleomorphic adenoma, oncocytomas, adenoid cystic carcinomas, adenocarcinomas, and acinic cell carcinomas. The excretory duct reserve cells will give rise to squamous cell and mucoepidermoid carcinomas.

Therefore, excretory duct cells give rise to squamous cell carcinomas, intercalated duct cells give rise to pleomorphic adenomas, striated ducts give rise to oncocytomas, and acinar cells give rise to acinic cell carcinomas. They are slow growing and are not well encapsulated. This tumor occurs later in life. There is a male predominance.

The most common of the three is the basal cell adenoma. These tumors are well circumscribed and encapsulated. The treatment is a superficial parotidectomy with preservation of the facial nerve.

After the gland is removed and sent to the frozen section lab, it should be properly oriented and tagged for the pathologist. If there is a close margin, then patients should be observed for recurrence, particularly in the case of a pleomorphic adenoma. They are classified as either low-grade or highgrade malignancies. The low-grade form has a higher ratio of mucous cells to epidermoid cells and behaves like benign tumors.

In the case of high-grade tumors, there is a higher portion of epidermoid cells resembling a squamous cell carcinoma. The latter have a high propensity for metastasis. The neoplasms present as firm or hard masses attached to the surrounding tissue.

Adenocarcinomas lack keratin and therefore are easily differentiated from mucoepidermoid carcinomas. It is the most common malignancy of the submandibular and minor salivary glands. Adenoid cystic carcinomas are unpredictable and may remain quiescent for years. These tumors grow along perineural planes and have a high incidence of distant metastasis, particularly to the lungs.

There are three histologic types�cribriform, solid, and tubular. The solid form has the worst prognosis, and the cribriform is considered the most benign of the group.

They account for 0. The entire parotid gland is enlarged as well as regional lymph nodes. Fine-needle aspiration FNA with flow cytometry may assist in diagnosing this condition because the treatment consists of chemotherapy followed by radiation therapy.

Salivary gland neoplasms in the very young are rare. The most common is the mucoepidermoid carcinoma. Facial nerve monitoring is a useful means of identifying the facial nerve, particularly during difficult parotid gland surgery. Multiple peripheral probes are normally placed at four locations�at the region of the temporal branch that innervates the frontalis muscle, the region of the zygomatic branch that innervates the orbicularis oculi muscle, the region of the buccal branch that innervates the orbicularis oris muscle, and the region of marginal mandibular nerve that innervates the muscle of the depressor muscle of the lower lip.

When the major divisions of the facial nerve are stimulated distally, facial movement will be evident. If the pes anserinus is stimulated, all distal branches of the nerve will fire simultaneously. Because this monitoring equipment is readily available at most institutions, one should consider its use, particularly from a medicolegal standpoint. Occasionally, deep lobe parotid tumor may present, on examination, as a mass in the lateral pharyngeal wall.

This is primarily the result of a weakness in the stylomandibular membrane. The parotid gland has the highest incidence of salivary gland tumors. As the salivary gland gets smaller, the incidence of malignancies increases. Involvement of the facial nerve in the presence of a parotid mass is usually an indication that a malignant process is present. The degree of paralysis should be noted clinically, and preoperative photos should be taken for documentation.

The workup is based on the clinical history and physical findings on examination of the patient. In these patients, one should suspect a high index of suspicion for a parotid malignancy. A careful examination of the oral cavity, scalp, larynx, base of tongue, and pharynx by means of a flexible endoscopic exam should be performed to rule out other primary sites.

A thorough examination of the neck is important in order to determine if metastatic disease has spread beyond the parotid gland. FNA may be easily performed in the clinical setting. Contrast computed tomography CT and magnetic resonance imaging are helpful in determining the location and extent of the mass; however, benign pathology can give similar findings�poorly defined borders as well as enhancement.

FNAB is a useful diagnostic adjunct in the evaluation of masses in the head and neck. FNAB is highly dependent on the experience of the pathologist.

Therefore, its role in the evaluation of salivary gland tumors is somewhat controversial. It is an excellent method of differentiating between a benign lymphadenopathy and a malignant process. There is anywhere between 1 and more than 20 lymph nodes randomly distributed within the parotid gland. Occasionally, you may see either salivary gland ducts or acini Neisse Nicholson rest within the nodal tissue.

There are six stage groupings for parotid tumors. If the histopathologic diagnosis is unknown prior to surgery, the minimum surgical procedure that should be performed is a superficial parotidectomy with dissection and preservation of the facial nerve with intraoperative frozen sections. Enucleation of a parotid tumor mass should not be performed because of the high incidence of recurrence. If the frozen section diagnosis returns positive for a malignant tumor, there are multiple treatment options available depending on the type of tumor identified, the presence of lymph nodes, distant metastasis, and facial nerve involvement.

Group 1: T1 or T2N0 low-grade malignancies acinic cell carcinoma and low-grade mucoepidermoid carcinomas. A superficial parotidectomy is performed with preservation of the facial nerve. Group 2: T1 or T2N0 high-grade features high-grade mucoepidermoid carcinoma, adenocarcinoma, adenoid cystic carcinoma, squamous cell carcinoma, carcinoma expleomorphic, and malignant mixed tumors. If the nerve is involved, it should be resected and cable grafted with a sural nerve graft.

Group 3: T3N0 or and N1 high-grade cancers and recurrent cancers. If the tumor involves the facial nerve at the stylomastoid foramen, then a mastoidectomy with exposure of the facial nerve within the fallopian canal and resection of the nerve until negative margins are obtained.

Group 4: T4 category. First is a complete history and physical examination, with particular emphasis on the mouth, pharynx, thyroid, and other lymph node basins. The next step is either a computed tomography CT scan or magnetic resonance imaging MRI if the mass cannot be separated from important structures carotid pulse, etc. Where did it come from?

If the node is in the posterior triangle, the primary is more likely nasopharynx, esophagus, or thyroid.

However, nodes that lie just above the clavicle usually represent cancer of the lung or other sites stomach, prostate, etc. If examination of the above areas is difficult while the patient is awake, the above areas may be reexamined under general anesthesia.

If something is noted, then biopsies should be performed. If nothing is noted, then blind biopsies should be performed of the base of the tongue and the nasopharynx. Why not just excise the node, find out what the problem is, and go from there? Excisional biopsy should never be the initial diagnostic maneuver, unless absolutely necessary. If lymphoma or an unusual infection is present, but not suspected, the node may be mishandled when sent to pathology or microbiology.

If metastatic cancer is the problem, the biopsy creates scarring in the field, complicates subsequent management, and may be detrimental to survival. Open biopsy is a particularly bad choice if the lump is a carotid body tumor and not metastatic cancer. What is the treatment algorithm? First, the patient should undergo a CT, CT-positron emission tomography, or MRI scan to determine other sites of disease, both above and below the clavicles.

Then, if nothing else is found other than the involved cervical node, there are basically two choices. One is a functional or modified neck dissection, followed by postoperative irradiation to the neck and likely primary site s. The other choice is primary irradiation alone to the same areas, with close follow-up, reserving surgery for emergence of disease at a later time. Prognosis in such patients is primarily determined by the presence of metastatic disease and much less so by the primary tumor.

So, to be sure, one should reexamine the patient in 6�8 weeks to make sure the initial diagnosis was sound. Alternatively, if only lymphocytes are found, it may now be reasonable to excise the node for final diagnosis.

Thyroid cancer presenting as an enlarged cervical lymph node. Rapid access multidisciplinary lymph node diagnostic clinic analysis of patients. Br J Cancer. Management of lateral neck masses in adults. Malignant cervical lymphadenopathy: diagnostic accuracy of diffusion-weighted MR imaging. The diagnostic value of fine needle aspiration in parotid lumps. Ann R Coll Surg Engl. Metastatic carcinoma of the neck, primary unknown. Atlanta: American Cancer Society; Management of neck lumps�a triage model.

J Nucl Med. The initial or type I lesion, consisting of lipid deposits in the intima, has been well characterized in infants and children.

Fatty streaks or type II lesions are visible as yellow-colored streaks, patches, or spots on the intimal surface of arteries. Microscopically, they are characterized by the intracellular accumulation of lipid. A foam cell is any cell that has ingested lipids, thus giving the histologic appearance of a sudsy vacuole.

In general, a foam cell refers to a lipid-laden macrophage; however, other cells that uptake lipids, particularly vascular smooth muscle cells, also may be considered foam cells. Although the sequence of events is not always consistent, fatty streaks progress to type III or intermediate lesions.

This growth is characterized by extracellular pools of lipid, which are generally clinically occult. However, when the pools coalesce to create a core of extracellular lipid type IV lesion or atheroma , the blood vessel architecture has been altered sufficiently to become clinically overt.

With smooth muscle cell SMC proliferation and collagen deposition, the atheroma becomes a fibroatheroma type V. The fibroatheroma is characterized by thrombogenic surface defects that provoke intramural hemorrhage or intraluminal thrombus type V lesion , resulting in vessel occlusion, which, in the case of a coronary artery, results in myocardial infarction MI. In , Enos reported autopsy findings from United States male battle casualties in Korea average age, 22 years.

The classic risk factors include tobacco use, hyperlipidemia, hypertension, diabetes mellitus, and family history of cardiovascular disease. That is the million-dollar question. Do parallel pathways lead to a final atherosclerotic lesion, or do the apparently dissimilar risk factors activate signals that converge to a few dominant events, promoting the development of atherosclerosis?

Certainly, this question has broad therapeutic implications. It would be a lot easier to inhibit a single proximal point in this process rather than to treat multiple divergent, more distal cellular pathologic events. The premise that atherogenesis represents an exaggerated inflammatory, fibroproliferative response to injury has evolved into an attractive unifying hypothesis of vascular disease and repair. Mechanical, metabolic, and toxic insults may injure the vessel wall. The common denominator is endothelial injury.

Disruption of the endothelium not only results in endothelial cell dysfunction but also allows adhesion and transmigration of circulating monocytes, platelets, and T lymphocytes. Under the influence of cytokines and growth factors, vascular smooth muscle cells VSMCs adapt to a synthetic phenotype and begin proliferation and migration across the internal elastic lamina into the intimal layer.

Stimulated VSMCs allow the deposition of extracellular matrix, thus converting the initial lesion to a fibrous plaque. Is it just another random, nonclinically relevant marker of inflammation?

CRP is one of many acute phase proteins elaborated from hepatocytes on inflammatory stimulation. Originally isolated from the serum of patients with pneumonia, it has a high binding affinity for pneumococcal C-polysaccharide. Although CRP is best known as an active peptide by neutralizing foreign antigens, controlling tissue damage, and promoting tissue repair, it is increasingly considered a sensitive marker of inflammation.

Unlike other markers of inflammation, CRP levels are stable over long periods of time, have no diurnal variation, can be measured inexpensively with available high-sensitivity assays, and have shown specificity in predicting risk of cardiovascular events. Indeed, elevation of CRP levels might be more predictive of cardiac events than elevation of low-density lipoprotein LDL levels. These observations may influence therapy because nonhyperlipidemic patients with elevated CRP levels might benefit from aggressive statin 3-hydroxylmethylglutaryl [HMG]-reductase inhibitors therapy.

Injury is a catch-all word that includes physical injury, such as angioplasty, hypertension, shear forces atherosclerotic lesions typically occur at bifurcations , and other diverse insults, including viruses, bacteria, nicotine, homocysteine, and oxidized LDLs. The lipid hypothesis of atherosclerosis suggests that the cellular changes in atherosclerosis are reactive events in response to lipid infiltration.

Indeed, antilipid therapy is one of the few strategies that has induced regression of atherosclerosis in randomized, prospective clinical trials. Strong evidence also derives from patients with genetic hyperlipidemias; homozygotes rarely live beyond age 26 years. Often referred to as syndrome X, metabolic syndrome is a phenomenon in older, sedentary people who have hyperinsulinemia associated with elevated blood sugar, high blood pressure, and increased triglycerides with decreased high-density lipoprotein HDL cholesterol levels.

Clinically, such patients develop premature cardiovascular disease. Insulin resistance with elevated insulin levels, with or without overt diabetes, fuels important aspects of atherogenesis, including dyslipidemias, endothelial dysfunction, hypertension, and SMC proliferation. For the trivia fans, and not to be confused with your in-laws, a similar condition has been observed in overweight horses known as equine metabolic syndrome.

What is its association with atherosclerosis? Leptin is a hormone secreted by adipocytes that maintains homeostasis between energy stores and energy expenditure through regulation of appetite and food intake. Alterations in the signaling pathway of leptin, whether through leptin resistance or leptin depletion, can result in excessive food intake and obesity. Leptin is also proatherogenic. It signals proliferation of monocytes, promotes oxidative stress in the endothelial cell, and prompts hypertrophy and proliferation of vascular smooth muscle cells.

Antioxidant therapy with vitamins C and E and beta-carotene is intuitively sound. In vitro, these agents afford resistance of LDL to oxidation and reduce elaboration of vessel-injuring reactive oxygen species. Although descriptive, case-control, and prospective cohort studies have found inverse associations between the frequency of coronary artery disease CAD and dietary intake of antioxidant vitamins, randomized therapeutic trials thus far have exhibited no benefit of doing so.

What is Atherosclerosis? This amino acid intermediate in the metabolism of methionine is an essential amino acid in the synthesis of both animal and plant proteins. Excessive homocysteine in the vessel wall reacts with low-density proteins to create damaging reactive oxygen species. Epidemiologic evidence correlates elevated levels of homocysteine and decreased levels of folate with cardiovascular disease.

Folic acid, vitamins B12 and B6, and pyridoxine are important cofactors for the enzymatic processing of homocysteine. Indeed, the reduction in mortality from cardiovascular causes since has been correlated with the increase in vitamin B6 supplementation in the food supply. Although these supplements may decrease homocysteine levels, the expected decrease in cardiovascular events has not yet been documented in prospective, randomized clinical trials.

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