BALDANIYA RAJESHBHAI V.

Medicine 4th year CLERK

MED-19-42195

GENERAL DATA:

This is a case of R.V., 64 year old, female, filipino, who was born on November 8,
1958. Roman Catholic from Purok ilang ilang buer, Aguilar, pangasinan.

Patient consulted first time in R1MC on January 05, 2023 around 9:00 am

Informant : PATIENT

Reliability : 90%

CHIEF COMPLAINT: ABDOMINAL PAIN

HISTORY OF PRESENT ILLNESS:

2 weeks prior to admission, patient noted persistent right lower quadrant pain,
characterized as crampy, with a pain scale of 3-4/10, with no other associated
symptoms noted. No aggravating or relieving factors noted. No medications taken, no
consult was done.

On the interim, …

Few hours PTA, patient had right lower quadrant pain with a pain scale of 8/10,with no
other associated symptoms like nausea, vomiting, fever, melena, hematochezia.
Persistence of symptoms prompted consultation at the rural health unit in Mangaldan,
Pangasinan and was transferred to the institution.

PAST MEDICAL HISTORY:

● (+) Hypertension (2010) on losartan 50 mg OD

● (-) DM
● (-) PTB
 ● (+)NEPHROLITHIASIS (2020) No surgical history

FAMILY HISTORY:

● MOTHER: (+) HPN

● FATHER : (+) HPN
● No malignancy

PERSONAL AND SOCIAL:

● 33 years married
● Previous Smoker (1 to 2 sticks per day)
● Previous alcohol drinker (Stopped 2020)

REVIEW OF SYSTEMS:

GENERAL : (+) generalized body weakness (-) weight loss

GASTROINTESTINAL : (-) anorexia, (-)nausea/retching, (-) vomiting,

(-) dysphagia, (-) hematemesis, (-) indigestion,

(-) melena, (-) hematochezia, (-) heartburn,

(+) abdominal pain, (-) hernia, (-) hemorrhoids

GENITOURINARY : (-) dysuria, (-) hematuria, (-) incontinence, ( ) nocturia,

(-)urinary frequency, (-) dribbling, (-) kidney stones

PHYSICAL EXAMINATION
General Survey: Patient is conscious, coherent, cooperative, oriented to time and place
and not in cardiorespiratory distress

VITAL SIGNS:

● Blood Pressure: 130/90 mmHg

● Heart Rate: 89 bpm
● Respiratory Rate: 20 bpm
● Temperature: 36.8 o C
● SpO2: 98%

ABDOMEN :

Globular in shape, non distended, no rash, discoloration, spider angiomata, scars noted.
Normoactive active bowel sound. Noted direct and Rebound tenderness noted at
RLQ.

DRE : (-) SKIN TAG, (-) HEMORRHOIDS , GOOD SPHINCTER TONE, (-)MASS, (+)
MELENA

SALIENT FEATURES:

SUBJECTIVE OBJECTIVE

● Blood Pressure: 130/90 mmHg

● 64/F
● RLQ pain last 2 weeks
● Hypertensive
● Nephrolithiasis 2020
● Smoker (1 to 2 sticks per day)
● Alcoholic before
● Heart Rate: 89 bpm
● Respiratory Rate: 20 bpm
● Temperature: 36.8 o C
● Spo2: 98%
● Direct and rebound tenderness at RLQ
DIAGNOSTICS:

CBC : Jan 09, 2023 8:30 am

WBC N L M E B RBC HGB HCT MCV MCH MCHC PLT

24.9 86.3 7.1 4.9 1.3 0.4 3.8 97 0.31 81.8 25.5 312 602

Total protein 58 (low)

Albumin 27 (low)

Globulin 31

A/G Ratio 0.87 (low)

HBA1C 6.1

Creatinine 0.8

Total Bilirubin 23.94 (high)

Direct Bilirubin 13.68 (high)

Indirect Bilirubin 10.26

CHEST X-RAY :
WAB UTZ :

● Right pelvic complex mass as described, consider a periappendiceal

abscess formation
● Bile gravel
● Normal sonogram of the liver, pancreas, spleen, kidneys and urinary bladder
● Normal size anteverted uterus
CT-SCAN OF ABDOMEN :

● Fairly large, lobulated heterogeneously enhancing mass with ill-defined

margins and of necrosis involving the entire circumferential wall of the
proximal transverse colon with possible extension into the adjacent distal
ileum. Findings are suggestive of a neoplastic process with possible
concurrent perilesional abscess formation.
● Related extensive mesenteric fat stranding densities and nodal
involvement with adjacent muscular and subcutaneous inflammatory
changes, as detailed.
● Appendix is unremarkable
● Hepatic steatosis
● Contracted gallbladder with thin wall clarification and tiny cholelithiasis
PRIMARY IMPRESSION : PROXIMAL TRANSVERSE COLON TUMOR

MANAGEMENT :

‘E’ Exploratory laparotomy, Extended right hemicolectomy, double bowel

ilio-colostomy

INTRAOPERATIVE FINDINGS :
POST OPERATIVE :
POST-OPERATIVE DIAGNOSIS :

PROXIMAL TRANSVERSE COLON TUMOR RUPTURED WITH ABSCESS

HISTOPATHOLOGY FINDINGS:

Tumor site : Cecum, Right Ascending Colon

Microscopic : Tumor perforation Present

Histologic type : Poorly differentiated adenocarcinoma

Tumor extension : Tumor invade pericolic fat

Margins proximal (ileus) and distal (transverse) uninvolved by carcinoma

Lymphovascular invasion : Present

Perineural invasion : Not identified

Regional lymph nodes : 2/10 lymph nodes positive for tumor

Pathologic stage : pT3pN1b

Other findings: Serositis

FINAL DIAGNOSIS :

Poorly differentiated adenocarcinoma; hepatic flexure proximal transverse colon

with ruptured abscess ; stage pT3pN1bMx

DISCUSSION :

On the one hand, from an embryological standpoint, the proximal two-thirds of the
transverse colon are derived from the midgut and the distal one-third is derived from the
hindgut, and they are supplied by the middle and left colic artery, respectively. On the
other hand, from an anatomical point of view, the transverse colon is in close proximity
to upper abdominal vital structures, and is not fixed to the retroperitoneal structures.
Due to the anatomy and embryology complexity, it is a challenging and daunting
mission to mobilize and resect the transverse colon

ETIOLOGY :

● Colorectal cancer is a multifactorial disease process.

○ Genetic factors
○ Environmental exposures (including diet)
○ Inflammatory conditions of the digestive tract are all involved in the
development of colorectal cancer.

EPIDEMIOLOGY :

● On a global scale, colorectal cancer is the second most common cancer in

females and ranks third among males.
● Generally, transverse colon cancer (TCC) is defined as tumors located between
hepatic and splenic flexure, and is relatively rare, accounting for 10% of all colon
cancer
● Aging is the dominant risk factor for colorectal cancer, More than 90% of cases
diagnosed are in people older than age 50 years. This is the rationale for
initiating screening tests of asymptomatic patients at average risk of developing
colorectal cancer at age 50 years. habits, rectal bleeding, melena, unexplained
anemia, or weight loss require a thorough evaluation.
● Hereditary Risk Factors. Approximately 80% of colorectal cancers occur
sporadically, while 20% arise in patients with a known family history of colorectal
cancer.
● Environmental and Dietary Factors. Diets high in animal fat and low in fiber, high
in saturated or polyunsaturated fats increases risk of colorectal cancer. Ingestion
of calcium; selenium; vitamins A, C, and E; carotenoids; and plant phenols may
decrease the risk of developing colorectal cancer. Obesity and sedentary lifestyle
dramatically increase cancer-related mortality
● Inflammatory Bowel Disease. Patients with long-standing colitis from
inflammatory bowel disease are at increased risk for the development of
colorectal cancer.
● Other Risk Factors. Cigarette smoking is associated with an increased risk of
colonic adenomas, especially after more than 35 years of use. Patients with
 ureterosigmoidostomy may also be at increased risk for both adenoma and
carcinoma formation."
● Pelvic irradiation may increase the risk of developing rectal carcinoma.

PATHOPHYSIOLOGY :

Genetically, colorectal cancer represents a complex disease, and genetic alterations are
often associated with progression from premalignant lesion (adenoma) to invasive
adenocarcinoma.

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 the activation of oncogene c-myc and cyclin D1, which
drives the progression to malignant phenotype.

Other important genes in colon carcinogenesis include the 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 the p53 tumor suppressor gene confer resistance to
programmed cell death (apoptosis) and are thought to be late events in colon
carcinogenesis.

In addition to mutations, epigenetic events such as abnormal DNA methylation can also
cause silencing of tumor suppressor genes or activation of oncogenes. These events
compromise the genetic balance and ultimately lead to malignant transformation.

Cancer cells produce extracellular vesicles (EVs)—principally, microvesicles and

exosomes—that can promote the growth, survival, invasiveness, and metastatic activity
of tumors. The colorectal cancer cells in this model secrete exosomes that carry
immunosuppressive microRNAs; these block CD28 on T cells and CD80 on dendritic
cells that infiltrate the tumors, disabling T-cell–mediated anti-tumor immune response.

Further, these authors found that intravenous injections of tumor-secreted exosomes

without immunosuppressive microRNAs, in combination with immune checkpoint
inhibitors, resulted in an enhanced anti-tumor immune response. This offers a potential
therapeutic strategy for late-stage colorectal cancer.

SIGN AND SYMPTOMS :

● Colon cancer is now often detected during screening procedures. Common

clinical presentations include the following:
○ Iron-deficiency anemia
○ Rectal bleeding
○ Abdominal pain
○ Change in bowel habits
○ Intestinal obstruction or perforation
● Physical findings may include the following:
○ Early disease: Nonspecific findings (fatigue, weight loss) or none at all
○ More advanced disease: Abdominal tenderness, macroscopic rectal
bleeding, palpable abdominal mass, hepatomegaly, ascites
○

DIAGNOSIS :

● Laboratory studies that may be helpful include the following:

○ Complete blood count
○ Chemistries and liver function tests
○ Serum carcinoembryonic antigen
● Imaging studies that may facilitate staging include the following:
○ Chest radiography
○ Chest computed tomography
○ Abdominal barium study
○ Abdominal/pelvic CT
○ Contrast ultrasonography of the abdomen and liver
○ Abdominal/pelvic MRI
○ Positron emission tomography, including fusion PET-CT scan
● Other procedures that may be warranted include the following:
○ Colonoscopy
○ Sigmoidoscopy
 ○ Biopsy of suspicious lesions
○ Double-contrast barium enema

MANAGEMENT:

● Surgery is the only curative modality for

localized colon cancer (stage I-III). Surgical resection
potentially provides the only curative option for
patients with limited metastatic disease in liver
and/or lung (stage IV disease). Surgical options
include the following:
○ Right hemicolectomy
○ Extended right hemicolectomy
○ Left hemicolectomy
○ Sigmoid colectomy
○ Total abdominal colectomy with
ileorectal anastomosis

● Other therapeutic options for patients who are not surgical candidates include the
following:
● Cryotherapy
● Radiofrequency ablation
● Hepatic arterial infusion of chemotherapeutic agents
● Adjuvant (postoperative) therapy is used in selected patients with stage II colon
cancer who are at high risk of recurrence, and is standard for stage III colon
cancer.
● Regimens used for systemic chemotherapy may include the following:
○ 5-Fluorouracil (5-FU)
○ Capecitabine
○ Oxaliplatin
● Biologic agents employed to treat colon cancer include the following:
○ Bevacizumab (Avastin)
○ Cetuximab (Erbitux)
○ Ipilimumab (Yervoy)
○ Nivolumab (Opdivo)
○ Panitumumab (Vectibix)
○ Pembrolizumab (Keytruda)
○ Ramucirumab (Cyramza)