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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Case 8
Chief Complaint
“I have blood in my stool.”
History and Physical Examination
A 76-year-old man comes to the office for pre-operative evaluation of a mass found on the
left side of his colon. The patient came to attention several weeks ago because of fever.
His blood cultures grew Clostridium septicum, which elicited referral for colonoscopy,
the results of which showed the left-sided mass. Biopsy of the mass showed
adenocarcinoma of the colon
Physical examination reveals an alert older man in no distress. T is 98° F, pulse 86/min,
BP 112/72 mm Hg. Chest is clear and abdomen is soft and non-tender. Cardiovascular
exam is normal.
Differential Diagnosis
Initial Management
Setting: outpatient
Colon cancer: local1.
Colon cancer: metastatic2.
Hereditary non-polyposis colorectal cancer (HNPCC)3.
401
Diagnostic/Therapeutic Plan
Test Results
Assessment
When you find colon cancer that is local to the colon without metastases, you have a definite
chance of a real cure. Colonoscopy is meant to find cancers before they either spread locally
into the surrounding lymph nodes or more distantly into the liver, lungs, brain or bone. When
cancer is found early without spread to the nodes, cure by primary resection is possible
without the need for diverting colostomy.
Clostridium septicum and Streptococcus bovis are 2 organisms frequently associated with
colonic pathology, and when they are found, should always lead to an automatic colonoscopy.
The CEA in this case is not to diagnose colon cancer, but to be used to follow the response to
treatment. Resection of the cancer and adjuvant chemotherapy should result in a decrease in the
CEA level.
Abdominal CT
Carcinoembryonic antigen (CEA)
Surgical consultation
Oncology consultation
CBC
PT and aPTT
Abdominal CT: lesion limited to colon, no invasion of surrounding tissue; no liver or lung
metastases; surrounding nodes are normal in size.
CEA: elevated
CBC: hematocrit 32%, MCV 76 fl (low)
PT and aPTT: normal
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It is understandable that the person has microcytic anemia when presenting with blood in the
stool. Although you should order surgical and oncologic consultation on CCS, do not expect
any consultant to make a specific recommendation.
Further Management
Discussion
With a family history of colon cancer, perform colonoscopy in the children by age 40 or 10 yrs
earlier than the age at which the cancer occurred in the source patient. The interval should be
every 10 yrs when the family member is age ≥60 when they developed the cancer. If the source
patient had the cancer age <60 the family members should be screened every 5 yrs.
HNPCC is when there are 3 family members with colon cancer in at least 2 generations and
one person had it prematurely (which is age <50). In HNPCC, screening colonoscopy should
start at age 25 and be done every 1 to 2 yrs.
Risks for colon cancer also include the presence of a family history or a familial syndrome
such as familial adenomatous polyposis (FAP) where the incidence for malignancy approaches
100% by age 50. In FAP screening sigmoidoscopy should begin at age 12 and when malignancy
is seen a total colectomy is recommended. Current recommendations for normal risk patients
include yearly testing for fecal occult blood, which reduces mortality by 30 to 40%, and
flexible sigmoidoscopy every 3–5 yrs. Sigmoidoscopy can miss up to 50% of cancers that are
more proximal. Colonoscopy can be used instead of the sigmoidoscopy every 10 yrs. Patients
with a polyp identified should undergo a colonoscopy with a repeat 3 to 5 yrs later. Stool heme
testing should start at age 50 and be performed every year.
Colectomy (partial or complete)
Screening of family members
403
With IBD, screening colonoscopy should be done after 8 yrs of involvement of the colon. This
is with either Crohn’s disease or ulcerative colitis.
CCS NOTE
On CCS, you cannot physically move the patient to the operating room, but you can
order the procedure you feel is needed. Step 3 is a test of general medicine. It will
consider that you know to screen the family members as a more important action step
than a specific operative technique. The patient’s children should all be screened by
age 40.
Follow-up Management and Prevention
Summary of colon cancer screening:
Adjuvant chemotherapy after colectomy to remove micrometastases
Repeat CEA
Final Diagnosis
Colon cancer
General population: begin age 50, every 10 yrs colonoscopy
One family member: begin age 40, every 10 yrs colonoscopy
Three family members (HNPCC) begin age 25, yearly
FAP: begin age 12, yearly
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405
Case 9
Chief Complaint
“I’m tired and my belly hurts.”
History and Physical Examination
A 55-year-old, generally healthy man comes to the office for a follow-up visit of fatigue
and left upper quadrant abdominal pain. The fatigue has been slowly progressive over
several weeks. On his last visit, CBC showed WBC 157,000 mm
3
, hematocrit 31%, and
slightly elevated platelet count.
His BP is 110/70 mm Hg and pulse 75/min. He is afebrile. The chest is clear to
auscultation. Cardiovascular examination is normal. The abdomen shows fullness in the
left upper quadrant.
Differential Diagnosis
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Chronic lymphocytic leukemia (CLL)
1.
Chronic myelogenous leukemia (CML)
2.
Acute leukemia
3.
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Test Results
Assessment
Chronic fatigue is a nonspecific finding, and a CBC to exclude anemia is always a good place
to start. Elevated WBC in an afebrile, generally healthy person can be CML, CLL, or on
occasion, a reactive elevation to another infectious/inflammatory condition.
Acute leukemia can cause a high, low, or normal WBC. It would be highly unlikely for acute
leukemia to be the cause of an isolated elevation in WBC without abnormalities of the other
cell lines. CLL is usually seen in patients age >60, and it is easy to diagnose with the
differential on the CBC. The smear is great to exclude acute leukemia when there are no blasts
seen. The smear CML often shows a left-shifted pattern, with myelocytes at various stages of
maturation (myelocytes, metamyelocytes, etc.)
Sonography of the abdomen is important with the abdominal pain. CML often gives left upper
quadrant abdominal pain from spleen enlargement (splenomegly). This can also lead to early
satiety, which is the sense of ‘feeling full’ even though a person has eaten only a small amount
of food. This is caused by the spleen pressing on the stomach.
Differential of WBC
Peripheral smear
Abdominal U/S
PCR for BCR/ABL (Philadelphia chromosome translocation of 9:22)
95% neutrophils
Peripheral smear normal, no blasts
Enlarged spleen
PCR for BCR/ABL present
407
The leukocycte alkaline phosphatase (LAP) score is not typically needed to tell the difference
between leukemia and a reactive high WBC. LAP is elevated in a high WBC count that is
caused by infection. LAP score is low in leukemia because the cells are abnormal. Instead of
LAP score, we can do the PCR for the BCR/ABL mutation.
Further Management Plan/Results
Infiltration with large numbers of normal-
appearing neutrophils (<20% of total)
Discussion
CML is treated with imatinib, a highly effective tyrosine-kinase inhibitor. Imatinib has largely
eliminated the need for bone marrow transplantation. It is one of the great miracles of
medicine, i.e., a ‘miracle’ for those with CML. It takes death and transforms it to life.
CML had formerly been a disease with near 100% need for transplantation by 5 yrs after
diagnosis. CML has the highest rate of transformation to acute leukemia of any form of
leukemia.
Imatinib is a pill with minimal adverse effects. It has the ability to eliminate the Philadelphia
chromosome entirely in 60% of patients. Some 98% of patients achieve hematologic control
with imatinib, so bone marrow transplant is seldom used. (Thus, bone marrow transplant is
never the best initial therapy.)
The fundamental defect in CML is the Philadelphia chromosome, which is a translocation in
genetic material between chromosomes 9 and 22. When they fuse into a new chromosome, the
junction point is known as the BCR/ABL region. These are the most specific tests for CML.
The BCR/ABL produces tyrosine kinase, which drives the proliferation of the malignant cells.
Imatinib inhibits the tyrosine kinase produced by the Philadelphia chromosome or BCR/ABL
Bone marrow biopsy
1.
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and usually puts the patient into remission. Other, newer agents such as dasatinib, niltonib, and
ponatinib exist, but the first-line treatment is currently imatinib.
Follow-up Management
CLINICAL PEARL
CML
CLINICAL PEARL
CLL
Imatinib (Gleevec)
Bone marrow transplantation is curative, but generally not necessary; it is done only in the
small number of patients not controlled by imatinib or another tyrosine kinase inhibitor
If acute leukostasis reaction develops, e.g., shortness of breath, blurry vision, or confusion,
then leukapheresis can be used.
High WBC with normal-appearing neutrophils and maturing neutrophils in
peripheral blood
Philadelphia chromosome and BCR/ABL are present
Treat with the tyrosine kinase inhibitor, imatinib
Bone marrow transplantation is curative if non-responsive to tyrosine-kinase
inhibitors
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Final Diagnosis
Chronic myelogenous leukemia
Exclusively in older patients
High WBC count that is all lymphocytes
Smear is generally normal, except for ‘smudge’ cells, which are essentially an
artifact
Treat with fludarabine, rituximab, cyclophosphamide, bendamustine, or
chlorambucil
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