Motion sickness

1) What is INR and its indication?

INR (International normalized ratio)
The international normalized ratio (INR), prothrombin ratio (PR) and prothrombin time (PT) are
measures of the extrinsic pathway of coagulation, measures the time ittakes for blood to clot and
compares it to an average.They are used in the measure of warfarin dosage, liver damage and vitamin
K status.PT measures the extrinsic pathway coagulation which is made up of Clotting factors: I, II, V,
VII, and X. The reference range for prothrombin time is 7-10 seconds, the range for the INR is 0.8-1.2.
The higher the INR, the longer it takes blood to clot and the closer the ratio to one meaning it is closer
to normal PT. An INR can be too high; a number greater than 4.0 may indicate that blood is clotting
too slowly, creating a risk of uncontrolled bleeding.

2) Step-ladder appearance , riegler’ sign.

Step ladder sign.

The appearance of multiple air-fluid levels on erect abdominal film is sometimes referred to
as a step ladder sign.

Rigler's sign
Rigler's sign, also known as the double wall sign, is seen on an x-ray of the abdomen when air is present on
both sides of the intestine; a Rigler's sign is present when air is present on the inside (lumenal side) and the
outside (peritoneal side). Gas normally outlines only the luminal surface of the bowel wall and not
the serosal surface, which has a degree of opacity similar to that of adjacent peritoneal
contents. When at least a moderate amount of free intraperitoneal air exists, however, this free
air is more likely to accumulate between bowel loops, thus permitting visualization of the outer
walls of the bowel. This is the classic appearance of the Rigler sign Air in the peritoneum is

considered abnormal, unless the patient had a recent abdominal surgery. A false double wall sign can result
from two loops of bowel being in contact with one another.[1] The sign is named after Leo George Rigler.

3) SBO

Background
Bowel obstruction (or intestinal obstruction) is a mechanical or functional obstruction of the intestines,
preventing the normal transit of the products of digestion. It can occur at any level distal to
the duodenum of the small intestine and is a medical emergency
SBOs can be partial or complete, simple (ie, nonstrangulated) or strangulated. Strangulated obstructions
are surgical emergencies. If not diagnosed and properly treated, vascular compromise leads to bowel
ischemia and further morbidity and mortality. Because as many as 40% of patients have strangulated
obstructions, differentiating the characteristics and etiologies of obstruction is critical to proper patient
treatment

Pathophysiology
Obstruction of the small bowel leads to proximal dilatation of the intestine due to accumulation of GI
secretions and swallowed air. This bowel dilatation stimulates cell secretory activity resulting in more fluid
accumulation. This leads to increased peristalsis both above and below the obstruction with frequent
loose stools and flatus early in its course.

Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to
increased intraluminal pressures. This can cause compression of mucosal lymphatics leading to bowel
wall lymphedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure in
the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal
lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity
and mortality.

Strangulated SBOs are most commonly associated with adhesions and occur when a loop of distended
bowel twists on its mesenteric pedicle. The arterial occlusion leads to bowel ischemia and necrosis. If left
untreated, this progresses to perforation, peritonitis, and death.

Bacteria in the gut proliferate proximal to the obstruction. Microvascular changes in the bowel wall allow
translocation to the mesenteric lymph nodes. This is associated with an increase in incidence of
bacteremia due to Escherichia coli, but the clinical significance is unclear.

Frequency
Mortality/Morbidity
Mortality and morbidity are dependent on the early recognition and correct diagnosis of obstruction. If
untreated, strangulated obstructions cause death in 100% of patients. If surgery is performed within 36
hours, the mortality rate decreases to 8%. The mortality rate is 25% if the surgery is postponed beyond 36
hours in these patients.

Clinical

History
Obstruction can be characterized as either partial or complete versus simple or strangulated.

 Abdominal pain (characteristic with most patients)

o Pain, often described as crampy and intermittent, is more prevalent in simple obstruction.
o Often, the presentation may provide clues to the approximate location and nature of the
obstruction. Usually, pain that occurs for a shorter duration of time and is colicky and
accompanied by bilious vomiting may be more proximal. Pain lasting as many as several
days, which is progressive in nature and with abdominal distention, may be typical of a
more distal obstruction.
 o Changes in the character of the pain may indicate the development of a more serious
complication (ie, constant pain of strangulated or ischemic bowel).
 Nausea
 Vomiting, which is associated more with proximal obstructions
 Diarrhea (an early finding)
 Constipation (a late finding) as evidenced by the absence of flatus or bowel movements
 Fever and tachycardia - Occur late and may be associated with strangulation
 Previous abdominal or pelvic surgery,  previous radiation therapy, or both (may be part of
patient's medical history)
 History of malignancy (particularly ovarian and colonic)

Physical

 Abdominal distention
o Duodenal or proximal small bowel has less distention when obstructed than the distal
bowel has when obstructed.
o Hyperactive bowel sounds occur early as GI contents attempt to overcome the
obstruction.
o Hypoactive bowel sounds occur late.
o Exclude incarcerated hernias of the groin, femoral triangle, and obturator foramina.
o Proper genitourinary and pelvic examinations are essential.
o Look for the following during rectal examination:
 Gross or occult blood, which suggests late strangulation or malignancy
 Masses, which suggest obturator hernia
o Check for symptoms commonly believed to be more diagnostic of intestinal ischemia,
including the following:
 Fever (temperature >100°F)
 Tachycardia (>100 beats/min)
 Peritoneal signs
o No reliable way exists to differentiate simple from early strangulated obstruction on
physical examination. Serial abdominal examinations are important and may detect
changes early.

Causes

 The most common cause of SBO is postsurgical adhesions.

o Postoperative adhesions can be the cause of acute obstruction within 4 weeks of surgery
or of chronic obstruction decades later.
o The second most common identified cause of SBO is an incarcerated groin hernia.
 The causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and
intussusception.

.  Hernias: A hernia is an abnormal protrusion of bowel through an opening. If the bowel protrudes, for example,
through the inguinal canal into scrotum, the intestinal lumen can be narrowed, preventing the passage of food.

 Cancers: Primary small bowel cancer is very rare, causing less than 3% of small bowel obstructions. However,
other cancers like melanoma can metastasize to the small bowel. If the tumor within the wall of the small bowel grows
large enough, it can occlude the lumen and cause an obstruction. In addition to primary small bowel tumors and
metastases, a small bowel obstruction can also be caused by direct invasion of a cancer from a nearby location
(colon, bladder, etc.)
 Crohn's disease: Causes strictures, or narrowings, within the small bowel. If severe, these strictures can cause an
obstruction.
 Volvulus: A twisting of the intestine. This can cause a "closed loop obstruction," in which gas or secretions cannot
escape the twisted segment either proximally or distally. This can result quickly in strangulation, necrosis (cell death),
and perforation of the intestines!
 Intussusception
 Intestinal strictures (narrowings) caused by radiation therapy (for cancer)
 Foreign body: If a child swallows a large marble, for example.
 Gallstone ileus
 Hematoma: A collection of blood within the wall of the intestines. If the hematoma expands, it can narrow and
block of the lumen (opening) of the intestines, causing a small bowel obstruction.
Workup

Laboratory Studies

 Essential laboratory tests

o Serum chemistries: Results are usually normal or mildly elevated.
o BUN level: If the BUN level is increased, this may indicate decreased volume state (eg,
dehydration).
o Creatinine level: Creatinine level elevations may indicate dehydration.
o CBC: WBC count may be elevated with a left shift in simple or strangulated obstructions.
Increased hematocrit is an indicator of volume state (ie, dehydration).
o Lactate dehydrogenase tests
o Urinalysis
o Type and crossmatch: The patient may require surgical intervention.
 Laboratory tests to exclude biliary or hepatic disease
o Phosphate level
o Creatine kinase level
o Liver panels

Imaging Studies

 Plain radiography.
o Plain radiography is of little assistance in differentiating strangulation from simple
obstruction. Some have used abdominal radiography to distinguish between complete
obstruction and partial or no SBO. A study by Lappas et al proposed that 2 findings were
more predictive of a higher grade or complete SBO: presence of air-fluid differential
height in the same small-bowel loop and presence of a mean level width greater than 25
mm.1 The study found that when the 2 findings are present, the obstruction is most likely
high grade or complete. When both are absent, the authors proposed that a low-grade
(partial) SBO is likely or nonexistent.
o Dilated small-bowel loops with air fluid levels indicate SBO.
o Absent or minimal colonic gas indicates SBO.
 Enteroclysis
o Enteroclysis is a fluoroscopic X-ray of the small intestine. Radiocontrast is infused
through a tube inserted through the nose to the duodenum, and images are taken in real
time as the contrast moves through aided by administration of methyl cellulose
 o Enteroclysis is valuable in detecting the presence of obstruction and in differentiating
partial from complete blockages.
o This study is useful when plain radiographic findings are normal in the presence of
clinical signs of SBO or if plain radiographic findings are nonspecific.
o It distinguishes adhesions from metastases, tumor recurrence, and radiation damage.
o Enteroclysis offers a high negative predictive value and can be performed with 2 types of
contrast.
o Barium is the classic contrast agent used in this study. It is safe and useful when
diagnosing obstructions provided no evidence of bowel ischemia or perforation exists.
Barium has been associated with peritonitis and should be avoided if perforation is
suspected.
 CT scanning
o CT scanning is useful in making an early diagnosis of strangulated obstruction and in
delineating the myriad other causes of acute abdominal pain, particularly when clinical
and radiographic findings are inconclusive. It also has proved useful in distinguishing the
etiologies of SBO, that is, extrinsic causes such as adhesions and hernia from intrinsic
causes such as neoplasms or Crohn disease. It also differentiates the above from
intraluminal causes such as bezoars.
o CT scanning is about 90% sensitive and specific in detecting SBO.
o It is capable of revealing abscess, inflammatory process, extraluminal pathology resulting
in obstruction, and mesenteric ischemia.
o CT scanning enables the clinician to distinguish between ileus and mechanical small
bowel in postoperative patients.
o CT scanning does not require oral contrast for the diagnosis of SBO because the
retained intraluminal fluid serves as a natural contrast agent.
o Obstruction is present if the small-bowel loop is greater than 2.5 cm in diameter dilated
proximal to a distinct transition zone of collapsed bowel less than 1 cm in diameter.
o A smooth beak indicates simple obstruction without vascular compromise; a serrated
beak may indicate strangulation.
o Bowel wall thickening indicates early strangulation.
o Portal venous gas indicates early strangulation.
o Pneumatosis indicates early strangulation.
o CT scanning is useful in identifying abscesses, hernias, and tumors.
o CT may be less useful in the evaluation of small bowel ischemia associated with
obstruction.
o One small series reported a sensitivity of 93%, specificity of 100%, and accuracy of 94%
in detecting obstruction. Another reported a sensitivity of 92% and specificity of 71% in
correct identification of partial or complete SBO.
 CT enterography (CT enteroclysis)
o This modality is replacing enteroclysis in clinical practice.2,3,4
o This is also the examination of choice for intermittent SBO or in patients with complicated
surgical history (eg, prior surgery, tumors).5
o It displays the entire thickness of the bowel wall and allows evaluation of surrounding
mesentery and perinephric fat.2
o Newer imaging technique that uses CT technology to perform thin slices of bowel along
while simultaneously using large volume enteric contrast material for imagery.2
o More accurate than conventional CT at finding cause of SBO (89% vs 50%), as well as
locating site (100% vs 94%).6
 o Helpful in patients being managed conservatively (ie, nonoperatively).6
 MRI
o The accuracy of MRI almost approaches that of CT scanning for detection of obstruction.2
o MRI is also effective in defining location and etiology of obstruction.7
o MRI has several limitations, such as lack of availability (transporting sicker patients is
difficult) and poor visualization of masses or inflammation.8,9
 Ultrasonography
o Ultrasonography is less costly and less invasive than CT scanning.
o It may reliably exclude SBO in as many as 89% of patients.
o Specificity is reportedly 100%.

Procedures

 Nasogastric tube placement and suction should be performed for patients with severe nausea
and vomiting.

Emergency Department Care

Initial ED treatment consists of aggressive fluid resuscitation, bowel decompression, administration of
analgesia and antiemetic as indicated clinically, antibiotics, and early surgical consultation.

 Initial decompression can be performed by placement of a nasogastric (NG) tube for suctioning
GI contents and preventing aspiration.
 Antibiotics are used to cover against gram-negative and anaerobic organisms.
 Monitor airway, breathing, and circulation (ABCs).
o Blood pressure monitoring
o Cardiac monitoring in selected patients (especially elderly patients or those with comorbid
conditions)

Consultations

 General surgeon (early and without delay): Laparoscopy is being used in addition to laparotomy
and has been shown to reduce hospital stay, speed recovery, and decrease morbidity.

Medication

Fluid replacement with aggressive intravenous resuscitation using isotonic saline or lactated Ringer
solution is indicated. Oxygen and appropriate monitoring are also required. Antibiotics are used to cover
gram-negative and anaerobic organisms.

Antibiotics
These agents are for prophylaxis in surgical intervention, if needed.

Complications

 Sepsis
 Intra-abdominal abscess
 Wound dehiscence
  Aspiration
 Short-bowel syndrome (as a result of multiple surgeries)
 Death (secondary to delayed treatment)

Prognosis

 With proper diagnosis and treatment of the obstruction, prognosis is good. Complete obstructions
treated successfully nonoperatively have a higher incidence of recurrence than those treated
surgically.

4) Differences between small and large bowel obstruction ?(signs and symptoms, clinical
findings, x-ray)
5) Staging of colorectal cancer.

Original Dukes Staging system

Dukes A: Invasion into but not through the bowel wall
Dukes B: Invasion through the bowel wall but not involving lymph nodes
Dukes C: Involvement of lymph nodes
Dukes D: Widespread metastases

Modified Dukes Staging System for Colorectal Cancer, with An adaptation by the Americans Astler and
Coller in 1954 further divided stages B and C[4]
Modified
The tumor penetrates into the mucosa of the bowel wall but no further.
Dukes A

Modified B1: tumor penetrates into, but not through the muscularis propria (the
Dukes B muscular layer) of the bowel wall.B2: tumor penetrates into and through the
muscularis propria of the bowel wall.

Modified C1: tumor penetrates into, but not through the muscularis propria of the bowel
Dukes C wall; there is pathologic evidence of colon cancer in the lymph nodes. C2:
tumor penetrates into and through the muscularis propria of the bowel wall;
there is pathologic evidence of colon cancer in the lymph nodes.

Modified The tumor, which has spread beyond the confines of the lymph nodes (to
Dukes D organs such as the liver, lung or bone).

TNM (Tumor, Node, Metastasis) Staging System for Colorectal Cancer

Tumor

T1: Tumor invades submucosa. 

T2: Tumor invades muscularis propria. 
T3: Tumor invades through the muscularis propria into the subserosa, or into the pericolic or perirectal
tissues. 
T4: Tumor directly invades other organs or structures, and/or perforates.
Node

N0: No regional lymph node metastasis. 

N1: Metastasis in 1 to 3 regional lymph nodes. 
N2: Metastasis in 4 or more regional lymph nodes.

Metastasis

M0: No distant metastasis. 

M1: Distant metastasis present.

Colorectal Cancer Stage Groupings

Stage I: T1 N0 M0; T2 N0 M0 

Cancer has begun to spread, but is still in the inner lining.

Stage II: T3 N0 M0; T4 N0 M0 

Cancer has spread to other organs near the colon or rectum. It has not reached lymph nodes.

Stage III: any T, N1-2, M0 

Cancer has spread to lymph nodes, but has not been carried to distant parts of the body.

Stage IV: any T, any N, M1 

Cancer has been carried through the lymph system to distant parts of the body. This is known as metastasis. The
most likely organs to experience metastasis from colorectal cancer are the lungs and liver.

6) Adenocarcinoma of bowel

Background
Almost all colon cancers are primary adenocarcinomas, which are the third most common cancer in both
men and women in North America and Western Europe.  More than 940,000 new cases of colorectal
cancer and nearly 500,000 deaths associated with colorectal cancer are reported worldwide each year
(World Health Organization, 2003).

Pathophysiology

i) APC/b-Cathenin pathway

The early event is a mutation of APC (adenomatous polyposis gene), which was first
discovered in individuals with familial adenomatous polyposis (FAP). The protein encoded
by APC is important in activation of oncogene c-myc and cyclin D1, which drives the
progression to malignant phenotype.

Other important genes in colon carcinogenesis include KRAS oncogene , chromosome 18

loss of heterozygosity (LOH) leading to inactivation of SMAD4 (DPC4), and DCC (deleted in
colon cancer) tumor suppression genes. Chromosome arm 17p deletion and mutations
 affecting p53 tumor suppressor gene confer resistance to programmed cell death (apoptosis)
and are thought to be late events in colon carcinogenesis.

ii) Microsatellite instability

A subset of colorectal cancers is characterized with deficient DNA mismatch repair. This
phenotype has been linked to mutations of genes such as MSH2, MLH1, and PMS2. These
mutations result in so-called high frequency microsatellite instability (H-MSI), which can be
detected with an immunocytochemistry assay. H-MSI is a hallmark of hereditary nonpolyposis
colon cancer syndrome (HNPCC, Lynch syndrome), which accounts for about 6% of all colon
cancers. H-MSI is also found in about 20% of sporadic colon cancers.

Signs and Symptoms: 

 May be asymptomatic
 Microcytic hypochromic anemia (fatigue, shortness of breath, angina)
 Vague abdominal discomfort
 Change in bowel habit
 Palpable mass
 Rectal bleeding (overt or occult)
 Large bowel obstruction
 Perforation (rare)
 Jaundice
 Ascites

Pathology
The pathology of the tumor is usually reported from the analysis of tissue taken from a biopsy or
surgery. A pathology report will usually contain a description of cell type and grade. The most
common colon cancer cell type is adenocarcinoma which accounts for 95% of cases. Other, rarer
types includelymphoma and squamous cell carcinoma.

Gross:

Cancers on the right side (ascending colon and cecum) tend to be exophytic, that is, the tumour grows
outwards from one location in the bowel wall. This very rarely causes obstruction of feces, and presents
with symptoms such as anemia. Left-sided tumours tend to be circumferential, and can obstruct the bowel
much like a napkin ring.

Adenocarcinoma is a malignant epithelial tumor, originating from glandular epithelium of the colorectal
mucosa. It invades the wall, infiltrating the muscularis mucosae, the submucosa and then the muscularis
propria. Tumor cells describe irregular tubular structures, harboring pluristratification, multiple lumens,
reduced stroma ("back to back" aspect).

Adenocarcinoma means that the cancer started in the gland cells in the lining of the bowel wall. The
gland cells normally produce mucus. Mucus is a slimy substance that makes it easier for the stool to
pass through the bowel.
There are one or two rare types of adenocarcinoma of the colon and rectum. They are called
mucinous tumours and signet ring tumours. These terms refer to how the cells look under the
microscope.

Mucinous tumours often have the cancer cells in pools of mucus. Signet ring tumours have mucus
inside the cells. The mucus pushes the nucleus (control centre) of the cell over to one side, giving
the tumour cell a signet ring shape under the microscope. Only about 1 to 2% of all colorectal
cancers are the signet ring type. They are treated the same way as other adenocarcinomas of the
colon or rectum.

Sometimes, tumor cells are discohesive and secrete mucus, which invades the interstitium producing
large pools of mucus/colloid (optically "empty" spaces) - mucinous (colloid) adenocarcinoma, poorly
differentiated. If the mucus remains inside the tumor cell, it pushes the nucleus at the periphery - "signet-
ring cell." Depending on glandular architecture, cellular pleomorphism, and mucosecretion of the
predominant pattern, adenocarcinoma may present three degrees of differentiation: well, moderately, and
poorly differentiated.[44]

Most colorectal cancer tumors are thought to be cyclooxygenase-2 (COX-2) positive. This enzyme is
generally not found in healthy colon tissue, but is thought to fuel abnormal cell growth.
Preferred Examination

 Begin the evaluation with a history and physical examination, including a digital rectal
examination.
 Inspect the stool, and test for occult blood.
 Perform blood tests, including a full blood count, liver function tests, and carcinoembryonic
antigen (CEA) level.
 Perform either a sigmoidoscopy (rigid or flexible), along with a double-contrast barium enema
study, or a colonoscopy.
 CT scan colonography or virtual colonoscopy, to evaluate the entire colon, is described in CT
scan section of this article.

Several factors increase the risk for colonic cancer.

 High-fat, low-fiber diet

 Patient age greater than 50 years
 Personal history of colorectal adenoma or carcinoma (3-fold risk)
 First-degree relative with colorectal cancer (3-fold risk)
 Familial polyposis coli, Gardner syndrome, and Turcot syndrome (all patients develop colorectal
carcinoma unless they undergo a colectomy)
 Juvenile polyposis syndrome, Peutz-Jeghers syndrome, and Muir-Torre syndrome (risk increased
slightly)
 Hereditary nonpolyposis colorectal cancer (as many as 50% of patients are affected)
 Inflammatory bowel disease
o Ulcerative colitis (risk is 30% after 25 years)
o Crohn disease (4- to 10-fold risk)