Photographic Sequence 1 of 12.

Mesenteric Ischemia

 This 74 year-old male presents in our office with a vague
 abdominal pain and no additional complaints pain is
 described as diffuse located primarily in the lower abdomen.
 the whtte cell count was 24.500 with 90% neutrofils.

Click here to enlarge the image

Photographic Sequence 2 of 12.

 Patients with mesenteric ischemia have a rare, potentially
 life-threatening disease and may present to the primary
 care or emergency medicine physician. Acute and chronic
 forms of mesenteric ischemia share many similarities and
 have many differences.

 Click Here to enlarge the image.

Photographic Sequence 3 of 12.

 While acute mesenteric ischemia is a surgical emergency,
 patients with chronic mesenteric ischemia typically present
 with a more benign process. The specific causes of
 mesenteric ischemia include the following:

• Acute thrombotic and acute embolic mesenteric artery ischemia
• Visceral venous thrombosis
• Chronic mesenteric ischemia
• Nonocclusive mesenteric ischemia.

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Photographic Sequence 4 of 12.

 Acute mesenteric ischemia is interruption of intestinal
 blood flow by embolism, thrombosis, or a low-flow state. It
 leads to mediator release, inflammation, and ultimately
 infarction. Abdominal pain is out of proportion to physical
 findings. Early diagnosis is difficult, but angiography and
 exploratory laparotomy have the most sensitivity; other
 imaging modalities often become positive only late in the
 disease. Treatment is by embolectomy, revascularization of
 viable segments, or resection; sometimes vasodilator
 therapy is successful. Mortality is high.

 Click Here to Enlarge the Image

Photographic Sequence 5 of 12.

Etiology and Pathophysiology

 The intestinal mucosa has a high metabolic rate and,
 accordingly, a high blood flow requirement (normally
 receiving 20 to 25% of cardiac output), making it very
 sensitive to the effects of decreased perfusion. Ischemia
 disrupts the mucosal barrier, allowing release of bacteria,
 toxins, and vasoactive mediators, which in turn leads to
 myocardial depression, systemic inflammatory response
 syndrome (see Sepsis and Septic Shock), multisystem
 organ failure, and death. Mediator release may occur even
 before complete infarction. Necrosis can occur as soon as
 10 to 12 h after the onset of symptoms.

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Photographic Sequence 6 of 12.

 Three major vessels serve the abdominal contents: the
 celiac trunk, the superior mesenteric artery (SMA), and
 the inferior mesenteric artery (IMA). The celiac trunk
 supplies the esophagus, stomach, proximal duodenum,
 liver, gallbladder, pancreas, and spleen. The SMA supplies
 the distal duodenum, jejunum, ileum, and colon to the
 splenic flexure. The IMA supplies the descending colon
 and sigmoid colon and the rectum. Collateral vessels are
 abundant in the stomach, duodenum, and rectum; these
 areas rarely develop ischemia. The splenic flexure is a
 watershed between the SMA and IMA and is at particular
 risk of ischemia.

Photographic Sequence 7 of 12.

Causes of Acute Mesenteric Ischemia
Occlusion Type	Risk Factors
Arterial embolus (> 50%)	Coronary artery disease, heart failure, valvular heart disease, atrial fibrillation, history of arterial emboli
Arterial thrombosis (10%)	Generalized atherosclerosis
Venous thrombosis (5–15%)	Hypercoagulable state, inflammatory conditions (eg, pancreatitis, diverticulitis), trauma, heart failure, renal failure, portal hypertension, decompression sickness
Nonocclusive ischemia (25%)	Low flow states (eg, heart failure, shock, cardiopulmonary bypass) and splanchnic vasoconstriction (eg, vasopressors, cocaine)

Photographic Sequence 8 of 12.

Symptoms and Signs

 The early hallmark of mesenteric ischemia is severe pain
 but minimal physical findings. The abdomen remains soft,
 with little or no tenderness. Mild tachycardia may be
 present. Later, as necrosis develops, signs of peritonitis
 appear, with marked abdominal tenderness, guarding,
 rigidity, and no bowel sounds. The stool may be
 heme-positive (increasingly likely as ischemia progresses).
 The usual signs of shock develop and are frequently
 followed by death.

 Sudden onset of pain suggests but is not diagnostic of an
 arterial embolism, whereas a more gradual onset is typical
 of venous thrombosis. Patients with a history of
 postprandial abdominal discomfort (which suggests
 intestinal angina) may have arterial thrombosis.

Photographic Sequence 9 of 12.

Diagnosis

• Clinical diagnosis more important than diagnostic tests
• Mesenteric angiography if diagnosis unclear.

 Frequency:

 Mesenteric ischemia accounts for 0.1% of all hospital
 admissions. Risk factors for this disease include
 atherosclerosis, arrhythmias, hypovolemia, congestive
 heart failure, recent myocardial infarction (MI), valvular
 disease, advanced age, and intra-abdominal malignancy.
 Mesenteric artery stenosis is found in 17.5% of
 independent elderly adults.

Photographic Sequence 10 of 12.

 Patients with mesenteric ischemia have a very typical
 presentation. However, the diagnosis may be overlooked
 because of the vague nature of the patients' symptoms.
 Depending on the type of mesenteric ischemia, patients
 may present with a variety of signs and symptoms.
 Patients may present with a history of postprandial pain,
 typically starting 20-30 minutes after their last meal, that
 may last up to 60-90 minutes. Because of this, they
 develop food fear and experience subsequent weight loss.
 Patients may be severely malnourished upon presentation.

  Diagnostic Tests:

• No reliable test
• Helpful adjuncts include
• ABG – acidosis indicates ischemia but only develops in 50%
• Lactic acid
• ● Amylase
• ● Creatine phosphokinase
• ● D-Dimer (100% sensitivity in one study with 38% specificity)
• ● Leukocytosis – greater than 15K supports diagnosis.

Photographic Sequence 11 of 12.

Prognosis

 If diagnosis and treatment take place before infarction
 occurs, mortality is low; after intestinal infarction,
 mortality approaches 70 to 90%. For this reason, clinical
 diagnosis of mesenteric ischemia should supersede
 diagnostic tests, which may delay treatment.

Photographic Sequence 12 of 12.

See this helpful Link: Diagnosis and Treatment of Acute Mesenteric Ischemia

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Photographic Sequence 1 of 3.

Appendiceal Carcinoid Tumor

 The prognosis of appendiceal carcinoids is best predicted
 by the size of the tumor. Tumors less than 2 cm in size
 (found in approximately 95 percent of patients) are
 unlikely to have metastasized when diagnosed. In contrast,
 up to 30 percent of larger tumors have already
 metastasized at diagnosis.

 To enlarge the image in a new window, click on it

Photographic Sequence 2 of 3.

 Carcinoid tumor of the appendix

 Appendix — Carcinoid tumors are the most common
 neoplasms in the appendix. Approximately 1 in 300
 appendixes contain a carcinoid tumor, almost always as a
 incidental finding. Appendiceal carcinoids are felt to arise
 from endocrine cells in the lamina propria and submucosa

 Metastatic Carcinoid Tumors and the Carcinoid
 Syndrome — As noted previously, 90
 percent of patients with the carcinoid syndrome have
 metastatic disease, typically to the liver. Exceptions are
 bronchial and ovarian tumors that can produce symptoms
 without metastasis. Patients with the carcinoid syndrome
 may benefit from therapies for the different components of
 the syndrome.

Photographic Sequence 3 of 3.

Carcinoid Tumor of the Appendix

 Most patients with appendiceal carcinoids are
 asymptomatic. Symptoms are more likely with large
 tumors, those located at the base of the appendix, and with
 metastatic disease. The majority of tumors are located in
 the distal one-third of the appendix where they are unlikely
 to cause obstruction. In approximately 10 percent of
 patients, tumors are located at the base, where they can
 cause obstruction, leading to appendicitis. Features of the
 carcinoid syndrome may be present in patients with tumors
 that have metastasized to the liver.

 The prognosis of appendiceal carcinoids is best predicted
 by the size of the tumor, and the presence or absence of
 nodal or distant metastases. Tumors less than 2 cm in size
 (found in approximately 95 percent of patients) are unlikely
 to have metastasized when diagnosed. In contrast, up to 30
 percent of larger tumors have already metastasized at
 diagnosis.

Photographic Sequence 1 of 5.

Lung Adenocarcinoma.

 This 72 year-old male with a long standing history of heavy
 smoking underwent a screening due to a dysphagia. The
 upper endoscopy was unremarkable.

Photographic Sequence 2 of 5.

 Computer Axial Tomography.

Download the video clip by clicking on the CT image.

Photographic Sequence 3 of 5.

 Large cell adenocarcinoma of the lung.
 (Microscopic detail).

Photographic Sequence 4 of 5.

Pleural retraction due to lung adenocarcinoma.

Photographic Sequence 5 of 5.

Pleural retraction due to lung adenocarcinoma.

Photographic Sequence 1 of 13.

Gallbladder Adenocarcinoma and litiasis.

 Gallbladder adenocarcinoma is an aggressive tumor and is
 one of the digestive tract malignancies with the poorest
 prognosis. Because of loco-regional extension and delayed
 diagnosis, curative resection is often impossible.

Photographic Sequence 2 of 13.

Gallbladder Adenocarcinoma and litiasis.

Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

 Although uncommon, carcinoma of the gallbladder (GB) is
 the most common primary hepatobiliary carcinoma, is the
 fifth most common malignancy of the GI tract, and
 predominantly affects older persons with long-standing
 cholecystolithiasis. GB epithelial tumors tend to behave
 similarly to other GI adenocarcinomas. When the diagnosis
 is made incidentally at the time of cholecystectomy,
 surgical resection can be curative; however, more
 commonly, the tumor is unresectable and rarely diagnosed
 preoperatively despite patients' symptoms. Early diagnosis
 can improve the clinical outcome and cure rate of GB
 carcinoma.

Photographic Sequence 3 of 13.

Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

 The exact etiology of GB carcinoma is unknown; however,
 several associated factors have been identified. One
 hypothesis suggests that irritation of the GB mucosa by
 stones causes chronic inflammation and, followed by
 repetitive epithelial repair, may cause malignant
 transformation. Approximately 15 years is required for
 dysplasia to progress to invasive carcinoma.

Photographic Sequence 4 of 13.

Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

Patients with GB carcinoma have an overall mean survival rate of 6 months, and the 5-year survival rate is 5%.

Photographic Sequence 5 of 13.

 Associated findings and risk factors for GB carcinoma are
 as follows:

 Several risk factors have been identified for GBC, many of
 which share a common characteristic of chronic gallbladder
 inflammationlamina propria and submucosa

• Cholecystolithiasis, which is present in 70-90% of patients (duration may be a key factor in development of cancer).
• Composition of the bile with cholesterol stones (most commonly implicated).
• Genetic factors.
• Calcification of the GB wall (carcinoma in 25% of patients with "porcelain" GB).
• Infections by Salmonella typhi.
• Environmental carcinogens.
• Gallbladder polyps
• Helicobacter — Helicobacter colonization of the biliary epithelium (particularly H. bilis) has been implicated in the pathogenesis of gallbladder disease including gallbladder cancer based upon detection of Helicobacter-derived cytotoxins and surface proteins using sensitive molecular and immunohistochemical techniques. The strength of this association requires further clarification.

Photographic Sequence 6 of 13.

 Gallbladder cancer (GBC) is an uncommon but highly fatal
 malignancy; fewer than 5000 new cases are diagnosed
 each year in the United States. The majority are found
 incidentally in patients undergoing exploration for
 cholelithiasis; a tumor will be found in 1 to 2 percent of
 such cases . The poor prognosis associated with GBC is
 thought to be related to advanced stage at diagnosis, which
 is due both to the anatomic position of the gallbladder, and
 the vagueness and nonspecificity of symptoms.

Photographic Sequence 7 of 13.

Microscopic pattern of gallblader carcinoma

Photographic Sequence 8 of 13.

 Microscopic detail of lymphatic and gallblader wall
 invasion.

Photographic Sequence 9 of 13.

Microscopic detail of lymphatic and gallblader wall
 invasion.

Photographic Sequence 10 of 13.

Photographic Sequence 11 of 13.

Photographic Sequence 12 of 13.

Photographic Sequence 13 of 13.

Giant Ovarian Serous Cystadenoma.

 This 35 year-old female, presented with voluminous serous
 cystadenoma of the ovary. She was treated surgically with
 good results.

To see more details on this case click here

Photographic Sequence 1 of 2.

Macronodular Cirrhosis

 Larger nodules separated by wider scars and irregularly
 distributed throughout the liver usually due to an infectious
 agent such as viral hepatitis which does not diffuse
 uniformly throughout the liver.

To enlarge the image click here

 Known causes of cirrhosis account for about 90-95% of
 the cases. Most common etiologies include alcoholism,
 autoimmune chronic hepatitis and chronic viral hepatitis.
 Less common causes include hemochromatosis, primary
 biliary cirrhosis, sclerosing cholangitis, drug-induced liver
 disease and chronic biliary obstruction. Other causes
 include a₁-antitrypsin deficiency, severe steatohepatitis in
 the morbidly obese and Wilson's disease. The remaining
 5-10% of patients with cirrhosis of the liver have no known
 cause, a condition termed cryptogenic cirrhosis. Over the
 last 10 years, the rate of cryptogenic cirrhosis has fallen
 from 30% to current levels. The most likely cause for this
 fall has been the availability of testing for hepatitis C.

 The etiology of the cirrhosis usually cannot be
 determined by the pathologic appearance of the liver
 (with some notable exceptions, including
 hemochromatosis and a₁-antitrypsin deficiency).
 Terms previously used such as portal cirrhosis or
 postnecrotic cirrhosis have been replaced
 by classifications that include three anatomic categories.

Photographic Sequence 2 of 2.

Classification of Cirrhosis

• Morphologic: Macronodular Micronodular Mixed
• Histologic: Portal, Post-necrotic, Post Hepatitic, Biliary, Congestive
• ETIOLOGIC AGENTS: Genetic, Toxic, Infectious, Biliary, Vascular, Cryptogenic

 This peculiar transformation of the liver was identified by
 the first anatomic pathologist, Gianbattista Morgagni in his
 500 autopsies published in 1761 but the name of
 "cirrhosis" (greek=orange color) was given by Laennec in
 1826 because of the yellowish-tan color of the cirrhotic liver
 . Only in 1930, one hundred years later, however, the first
 theory as to the pathogenesis of this disorder was
 advanced by Roessle: parenchymal degeneration,
 regeneration and scarring which is now understood
 according to the following sequence:

• Injury
• Degeneration
• Fibrosis
• Formation of fibro-vascular membranes
• Parenchymal dissection into nodules
• Rearrangement of blood
• Cirrhosis
  
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Photographic Sequence 1 of 5.

 Elephantiasis nostras verrucosa on the legs with morbid
 obesity.

 This 42 year-old male with morbid obesity more than 500
 libs. Came to our office to ask for help for weigh lost.

 Elephantiasis nostras verrucosa (ENV), is an unusual
 progressive cutaneous hypertrophy due to chronic
 lymphedema, and repeated inflammatory episodes. It
 usually manifests over the lower extremities as non-pitting
 edema with lichenification, hyperkeratotic papules,
 nodules, and verrucous, cobblestone-like plaques.

Photographic Sequence 2 of 5.

The condition has also been reported rarely on the upper extremities, ears, face, scrotum, chest, genitalia, buttocks, and periorbital region. Histolopathology shows acanthosis and hyperkeratosis of the epidermis and dilated lymphatic spaces in the dermis.

Photographic Sequence 3 of 5.

Elephantiasis nostras verrucosa represents longstanding obstruction of the lymphatic drainage, leading eventually to grotesque enlargement of the chronically dependent and immobile part(s) of the body.

 Chronic persistent lymphedema may lead to recurrent
 streptococcal lymphangitis, which can also be the
 predisposing factor. The microorganisms may gain entry
 into the lymphatics through minor injuries, interdigital
 fissures, or tinea pedis.

Photographic Sequence 4 of 5.

 Recurrence is common due to the protein rich edema. In
 the previous reports of abdominal ENV, it was
 hypothesized that the massiveness of the panniculus
 caused increased interstitial and intravascular pressure
 predisposing the patients to chronic low-grade cellulitis
 and lymphangitis.

Photographic Sequence 5 of 5.

 The condition may also occur secondary to trauma,
 surgery, tumor-obstruction, radiation, portal hypertension,
 congestive heart failure and Kaposi sarcoma. The
 differential diagnosis includes filariasis, pretibial
 myxedema, and stasis dermatitis. Obesity is a significant
 predisposing factor.

Photographic Sequence 1 of 2.

The Cullen sign, periumbilical ecchymosis

A faint blue discoloration around the umbilicus

 In acute pancreatitis, Cullen's or Turner's sign occurs in
 approximately 3 percent of patients and is associated with
 a mortality of 37 percent. Although most commonly
 described in hemorrhagic pancreatitis, neither of these
 signs is specific to this condition.

 Cullen's sign arises from the spread of retroperitoneal
 blood into the falciform ligament and subsequently to
 subcutaneous umbilical tissues through the connective
 tissue covering of the round ligament.

 Conditions Associated with Cullen’s Sign

• Pancreatitis
• Ruptured ectopic pregnancy
• Ruptured aortic aneurysm
• Ruptured spleen
• Ruptured common bile duct
• Perforated duodenal ulcer
• Hepatocellular carcinoma
• Hepatic lymphoma
• Metastatic thyroid cancer
• Rectus sheath hematoma

 

Photographic Sequence 2 of 2.

The Cullen sign of periumbilical ecchymosis is associated with retroperitoneal or abdominal wall hemorrhage.

 Definition: Periumbilical ecchymosis that typically occurs
 in the presence of hemoperitoneum, hemorrhagic
 pancreatitis, or uterine tube rupture in ectopic pregnancy.

 Physical findings: Bluish discoloration or ecchymosis
 around the umbilicus; abdominal tenderness may also be
 present in cases of significant intra-abdominal disease, and
 patients may also have flank ecchymosis (GreyTurner’s
 sign) if retroperitoneal bleeding is present.

 Cullen’s sign, or periumbilical ecchymosis, is associated
 with hemoperitoneum and may present with a myriad of
 disorders (Sidebar). First described by Cullen in 1918, this
 sign has become classically associated with hemorrhagic
 pancreatitis but can be seen with a host of other
 intra-abdominal processes. Grey Turner’s sign, or
 ecchymosis of the flanks,may also occur in conjunction
 with Cullen’s sign, especially in cases of retroperitoneal
 hemorrhage.