Manila
School of Medicine
Department of Pathology
Clinicopathologic Conference
Submitted by:
Group 6
Members:
BALDADO
CARINO
EZHILMARAN
KHAN
NASIR
PATRON
SANDOVAL
SILVERIO
TIONGSON
CHIVELA
April, 2018
I. Clinical Abstract
This is a case of 41-year old, a Filipino from Bulan, Sorsogon, with a chief complaint
of generalized body weakness and tarry stool.
➢ Review of Systems
- Positive weight loss of 50% in 2 months
- Early satiety
- Other findings unremarkable
➢ Physical Examination
- General: awake, coherent and in cardio respiratory distress
- Vital Sign: BP (90/60 mmHg), HR (86 bpm), body temperature (36.9).
Respiratory rate (21 cpm)
- HEENT: anicteric sclera, pink palpebral conjunctiva, moist lips, tongue and buccal
mucosa
- Chest / Lung: symmetrical chest expansion, no retraction, bronchovesicular breath
sounds in both upper lung files
- Heart: a dynamic precordium. normal rate, regular rhythm, point of maximal impulse
at 5th ICS LMCL, no murmur, heave or thrill
- Abdomen: flat abdomen with normoactive bowel sounds, direct tenderness on the
epigastric area, no splenomegaly
- Extremities: grossly normal with full equal pulses
➢ Neurologic Examination
- Unremarkable
Clinical Results
Chemistry
BUN Increased
Crea Normal
Na Decreased
K Normal
Chloride Normal
SGPT Normal
Cl Normal
TG Normal
TC Decrease
TB Normal
DB Increased
IB Normal
Microscopic:
Epithelial cells: Occasional
Mucus thread: Moderate
Amorphous urate: Many
WBC: 1-3/hpf
RBC: 0-2/hpf
Chemical:
Albumin: Trace
Sugar: Negative
Specific gravity: 1.010
pH: 6.0
Table 4. Radiology
Test Result
CXR PA PTB undetermined activity
Pulmonary nodule left
On the 24th hospital day, patient was drowsy by arousable. Intubated and hooked on
mechanical ventilator. CVP of 8-10 cm. Several hours, vital signs suddenly drop to zero. CPR
and ambubagging was done. Epinephrine were given. Patient revived with vital signs: BP
(palpatory 60), HR(84bpm), RR (gasping with low CBG. Dopamine drip was started
On the 25th hospital day, patient is unarousable with pupils dilated at 6mm. Patient
pronounced dead.
➢ Laboratory
- Leukocytosis
- Neutrophilia
- Lymphocytopenia
- Eosinopenia
- Decreased RBC, Hemoglobin, Hematocrit
- Increased RDW
- Decreased Platelet Ct
- Decreased MCV and MCH
- Increased BUN
- Decreased Na
- Increased Direct Bilirubin
➢ Radiology
- PTB undetermined activity
- Pulmonary nodule on left lung
- Minimal ascites
- Gallbladder Polyps
- Liver parenchymal disease superior left hepatic lobe 3.7x.3.2
- Pleural effusion
- Bilateral renal parenchymal disease
III. Clinical events chronology
In accordance with the symptoms listed, we as a team of clinical pathology students, will direct
our focus on the liver parenchyma, hepatobiliary tree and upper gastrointestinal tract
➢ Upper GIT
All clinical presentations seen in the case as very well consistent with chronic upper
gastrointestinal inflammatory processes, from non-neoplastic to neoplastic. Other probable
diagnosis in consideration is gastrointestinal TB.
The symptom of epigastric pain presented in the 2 months prior to admission is
consistent with upper GI involvement. This assumption comes with the fact that the patient has
pulmonary tuberculosis, and the epigastric pain may as well be a representation of a metastatic
phenomenon of the TB from the lungs, either via hematogenous spread or lymphatic spread.
Only CT scan and ultrasound will confirm our presumption. The upper GI involvement that we
refer to, if it presents with mucosa inflammation, may explain the bleeding that manifests as
melena or hematemesis, and again, the employment of endoscopic studies will confirm our
presumption.
For non-neoplastic, we considered metastatic tuberculosis, though primary
gastrointestinal tuberculosis is another acceptable differential for us as, since this is very well
consistent with the past illness of Pulmonary TB. No other non-neoplastic chronic differential
was found to be consistent with the case.
For neoplastic, we considered any gastrointestinal malignancy, we cannot specify
which, since the pathophysiologic description of either advanced localized or metastatic is that
of localized GI pain, and bleeding for most scenarios. And only endoscopy and histopathologic
studies will define what type of malignancy is in question. The involvement of the left lobe of
the liver, may have been associated with a transmural advance of the malignancy (most
possibly gastric cancer) into the liver parenchyma.
A possible secondary (metastatic) malignancy can also be considered. A metastatic
spread from anywhere near the viscera or even distant places may have occurred, and for that,
further diagnostic evaluation is to be done. In this same presumption, we considered the
possibility of a hepatocellular carcinoma involving the left lobe of the liver and spreading
directly to any gastrointestinal structure near the left side of the liver, and transmural invasion
of the structure in question and causing localized GI chronic inflammation and bleeding. To
confirm our clinical diagnosis, a CT scan and MRI studies will be needed.
➢ LIVER
The left hepatic lobe was found to be smaller than normal, this may indicate a chronic
inflammatory process that resulted in loss of normal parenchyma, and fibrosis (cirrhosis). The
inflammatory process may have had an underlying neoplastic or non-neoplastic disease.
For non-neoplastic, we considered metastatic tuberculosis to be the most consistent
cause for this case. The tuberculous complex from the lungs may have metastasized via
hematogenous or lymphatic spread from the lungs. Considering the location of the lesion
(localized), we consider rupture of a para-aortic tuberculous lymph node, invasion of the liver
capsule and consequent parenchymal infiltration of the superior left lobe of the liver. This may
be theoretically validated, in the fact that the liver is only partially involved, hence the near
normal liver function tests at the time of admission. The assumption may also explain the
epigastric pain, though it does not explain the upper GIT symptoms at first glimpse. The upper
GIT involvement, however, may be explained by the transmural invasion of the GI structures
surrounded by the same ruptured tuberculous lymph nodes, leading to chronic inflammation
and mucosal bleeding.
Alcoholic liver disease, is also brought into consideration for the fact that it is listed in
the patient’s history, that he was an alcoholic beverage drinker. The cirrhotic effect of alcohol
is well documented. The history is not specific on the patient's rate of alcohol consumption,
and the diagnostic test ordered only indicated minimal cirrhosis of the liver parenchyma.
Another important fact is that the data in the case only stated beginning of cirrhosis, without
further details on the degree of hepatic involvement. Hence, further diagnostic tests are to be
obtained in order to qualify cirrhosis secondary to chronic alcohol consumption. The liver
function tests are near normal, and this, theoretically, implies that the cirrhotic process is not
diffuse, rather localized. Yet, if the cirrhotic process proved to be diffuse, the finding would
explain the presence of gastrointestinal involvement (bleeding, chiefly) primarily stemming
from portal hypertension with underlying periportal hepatic fibrosis. The same finding would
also explain the Obstructive Jaundice caused by extrahepatic and/or intrahepatic bile duct
stenosis through ductal fibrosis.
For neoplastic, hepatocellular carcinoma came into light. The disease process depicted
by imaging studies for the case, as mentioned above, is a size decrease of the superior left lobe,
theoretically from cirrhosis. In this view, the underlying chronic inflammatory process is
elicited by the malignant proliferation of hepatocytes. It is well known that hepatocellular
carcinoma has its histologic variants, which can only be well characterized in histopathologic
studies. In this light, we assume that the neoplastic behavior is highly variable.
Notwithstanding, the presence of epigastric pain, may, therefore have its origin from the
neoplastic inflammation. The gastrointestinal involvement is explained either by the cirrhotic
effect on the portal vascular integrity, leading to gastrointestinal submucosal venous
congestion, and consequent bleeding, or, very unlikely, the direct spread of the hepatocellular
carcinoma into the adjacent gastrointestinal structure (transmurally) with mucosal extension
and consequent bleeding. The extra and/or intrahepatic biliary involvement, manifested with
the elevated ALP and direct bilirubin, stems from the inflammatory as well as cirrhotic on the
intrahepatic bile ducts
We considered the isolated involvement of the intra and/or extrahepatic bile ducts, in
the light of the facts that direct bilirubin is elevated as compared to indirect bilirubin, as well
as ALP is elevated, giving us the idea that the underlying cause may be inflammatory in nature,
as well as obstructive. Thus, non-neoplastic and neoplastic pathologic conditions come into
light.
For non-neoplastic, giving the case presentation, we make the diagnostic inclusion of
tuberculous choledocholangitis of metastatic nature, giving the history of primary pulmonary
tuberculosis. The inflammatory process elicits pain, thus explaining the epigastric pain
observed in the case. Chronic inflammation leads to stenosis of the bile ducts and cholestasis,
hence the elevated direct bilirubin and tea colored urine.
For Neoplastic conditions, we include any form of bile duct as well as gallbladder
neoplasia either primary (benign or malignant) or secondary, which can either be metastatic or
externally compressive. Neoplastic malignant nature is of most consideration, because of the
pain, most probably elicited by the chronic inflammation. Bile duct obstruction can be caused
by tumor growth into the lumen or by chronic inflammation resulting into ductal fibrosis and
stenosis. The result is the same as that of cholestasis, elevation of direct bilirubin as well as tea
colored urine, as noted in the case. A question may arise on how the upper gastrointestinal
symptoms of chronic bleeding came into existence.
V. DIFFERENGTIAL DIAGNOSIS
Having given our diagnostic work up, we made our differential diagnosis as the following:
1. Hepatocellular Carcinoma
4. Chronic Pancreatitis
5. Gastric Cancer
RATIONALE:
➢ Hepatocellular Carcinoma
In a study done by the department of internal medicine of the UP-PGH, the clinical
profile of hepatocellular carcinoma is that they occur more commonly in males (M:F 4:1), in
the age range of 29-86 (a mean age of 54), and that most of the patients complain is abdominal
pain. The patient was said to be an alcoholic drinker which could contribute to an increased
risk of developing hepatocellular carcinoma because of its effects on the liver, primarily
cirrhosis. There was also mention of the patient undergoing TB treatment and the anti-TB drugs
are known to be hepatotoxic.
Exposure to the risk factors mentioned above, can lead to chronic inflammation.
Inflammation may stimulate the visceral/peritoneal nerves causing pain. Epigastric pain is the
most common presentation seen in patients with hepatocellular carcinoma.
Risk Factors:
• Hepatitis B or Hepatitis C infection are the most common risk factors that have a strong
association with the development of HCC. There was no mention or laboratory to confirm
hepatitis infection.
• Alpha-1-antitrypsin deficiency and aflatoxin intake/use also have significant risk in
developing the disease which is absent in our patient.
Signs:
• Splenomegaly usually develops in the course of HCC.
• Jaundice is also absent which may be a sign of metastasis to the biliary tree
Diagnostics
• No mass seen on the whole abdominal ultrasound. A mass is usually seen in an abdominal
ultrasound but some might not be seen especially those less than 1cm or those who have a
diffuse-type HCC.
• The patient has normal SGPT (ALT) serum level. ALT is usually present in the heart and
in the liver. It becomes elevated when it is released into the blood as a result of damage. In
our case since we are considering HCC, there should be an elevated ALT serum level.
Hematologic findings which can correlate with the case would be presence of anemia
which is usually mild. Presence of Leukocytosis with neutrophilia found in our case can be
correlated to the Abdominal TB which is occasionally found as compared to the usual
lymphocytic type of Leukocytosis.
Hyperbilirubinemia Edema
Splenomegaly
Thrombocytopenia
According to Basra et al, alcohol induced hepatitis are seen in patients with alcohol
consumption history of over 80g of ethanol for over 5 years. However, the duration of drinking
before the onset of liver disease varies from 3months to 36 years as well as abstinence of more
than 3 months is unlikely to be associated with diagnosis of AH.
Specific signs and symptoms that can be seen in AH are Clinical jaundice (40-60% of
cases), hyperbilirubinemia which is considered a cardinal feature of the disease. Others also
report right upper quadrant pain, fever, tachycardia and tender enlarged liver. Other nonspecific
signs and symptoms such as nausea, vomiting, malaise and anorexia may also be related to
AH.
In severe cases, patients may present with hepatic encephalopathy, renal failure or
hepatorenal syndrome, ascites due to portal hypertension and bleeding tendencies due to
coagulopathy and thrombocytopenia. Malnutrition is also seen in 90% of patients with AH but
it can be due to Kwashiorkor or Marasmus.
➢ CHRONIC PANCREATITIS
Vomiting Hypercalcemia
➢ GASTROINTESTINAL SYMPTOMS
According to Malfertheiner et al., weight loss, dysphagia, signs and symptoms of upper
gastro-intestinal bleeding, anemia and persisting vomiting were the alarm symptoms that are
more frequently associated with upper gastro-intestinal malignancies. And immediate
endoscopy was recommended by most of the guidelines for all the patients presented with these
symptoms.3
➢ ANEMIA
Birgegard et al. stated that the result of complex interactions between tumor cells and
the immune system is cancer-related anemia. A shortened survival of red blood cells,
suppression of erythroid progenitor, impaired iron utilization and inadequate erythropoietin
production were the result of over expression of certain inflammatory cytokines.4
➢ ASCITES
Based on the journal of Saif et al, ascites is related to portal hypertension which is
usually related to liver cirrhosis. The major pathophysiologic mechanism in the formation of
ascites is the lymphatic obstruction, but there are evidences that suggest immunomodulators,
vascular permeability factors and metalloproteinase contribute significantly to the process.
Peripheral arterial vasodilation leading to underfilling of circulatory volume is the most
acceptable theory for the ascites formation. 8
➢ Neutrophilia
BUN and creatinine may be measured to check kidney function. Increase in both
parameters are indicative of metastasis of CA to the ureters or kidneys.
The Canadian Cancer Society states that lactate acid dehydrogenase, ALK,
transaminase and Bili can be measured to check liver function. An increase in these parameters
would also indicate metastasis to the liver.
Tomizawa et al suggest that BUN also represents products of protein metabolism via
ammonia. When GI bleeding happens, blood is digested to protein and the protein is then
transported to the liver via the portal vein and metabolized into BUN. Higher BUN values
mean increased digestion of blood.
Choyke et al states that bilateral renal metastases occur most commonly in the late
stages of malignancy. It is usually asymptomatic and hematuria or microhematuria are seen in
only 12-13% of patients. Lung cancer is the most common malignancy to have kidney
metastases, followed by breast cancer, gastric cancer and melanoma. However almost any late
stages can metastasize to the kidney.
✓ The chronic gastrointestinal bleeding causes a significant decrease in the blood volume.
✓ A possible metastasis to the liver lead to the inflammation of the affected hepatic
parenchyma and development of ascites.
✓ Back flow of blood into the gastrointestinal circulation led gastrointestinal vascular disease.
Gastrointestinal mucosal varices developed and ruptured, causing hemorrhage. This
explains the source of the bleeding manifested as melena/hematemesis, and the resulting
anemia.
✓ Hepatic hypoperfusion lead to hepatic dysfunction which decreased the protein synthesis
rate comprising of low erythropoietin (causing anemia) low thrombopoietin (causing
thrombocytopenia) low albumin (causing edema) and low lipoprotein (causing
hypocholesterolemia).
✓ Renal hypoperfusion lead to Acute Kidney Injury, manifested as decreased renal clearance
of nitrogenous wastes, increase in BUN, and ultimately uremia.
✓ From day 9 to day 12 Disseminated Intravascular coagulation was characteristic and was
defined progressive severe decrease in the platelet count and, although not recorded in the
lab results, abnormal PT and APTT which reflect consumptive coagulopathy.
✓ The hypoperfusion involves the heart, causing myocardial infarction and heart failure
✓ Accumulation of metabolites in the brain causes an increase in the glutamate activity. This
causes neurotoxicity and liquefactive necrosis, cerebral edema and an increase in the
intracranial pressure, altered sensorium and ultimately coma.
✓ Multiple organ failure from hypovolemic shock resulted in the demise of the patient.
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