CONTENT

NO TITLE PAGE

1 Acknowledgement 2

2 Overview of ascites 3-14

3 Case

1) Real case 15-21

2) Reference A 22-32

3) Reference B 33-42

4 Discussion 43-46

5 Conclusion 46

6
Reference 47

1
 ACKNOWLEDGEMENT

In the name of Allah, The Most Gracious, Most Merciful. All praises to Him for allowing me
to complete this case study within the allocated time. Peace and blessings on His Prophet
Muhammad and companions.

Firstly, I would like to extend my gratitude towards Hospital Slim River and its personnel for
giving me the opportunity to obtain invaluable experience in a friendly and supporting
environment, not to mention all the facilities provided for us.

Next, I would like to thank the dean of UniKL Mestech, Dr Reezal Ishak for giving us, DMA
students the golden opportunity to attach to this wonderful hospital for our clinical postings for
preparing us for the real working environment.

Also, credit to all DMA clinical lecturers, namely Mr Muhammad Norzein Ab Rahim, Mr
Zulaily Yacob, Mr Rahimy Hj Abdul Rahim, Mr Abdul Razak Sulaiman and Madam Siti Murni
Rosman for all the knowledges that they have shared throughout my studies.

In preparation of my assignment, I had to take the help and guidance of some respected persons,
who deserve my deepest gratitude. They are our clinical instructors who never back down from
giving us the utmost guidance, Mr Mahidzir Hassan and Madam Maimunah Ahmad, thank you
and may Allah bless you with His love and care.

I would also like to take this opportunity to thank all the members and staffs of the Emergency
Department,for all their help and encouragements throughout my posting there. Also, to my
friends and classmates, the patients, and everyone who helped me directly or indirectly, and
making it possible for me to complete this study.

Last but definitely not least, a big thank you to Kamarul Bin Adli, the patient of my real case
for the consent to be in this case study. May God grant you the health you are looking for.

Thank you.

2
Ascites (medscape reference)
Background
The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the
condition of pathologic fluid collection within the abdominal cavity. Healthy men have little
or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on
the phase of their menstrual cycle. This article focuses only on ascites associated with
cirrhosis.
See the image below.

This computed tomography scan demonstrates free intraperitoneal fluid due to urinary
ascites.
For excellent patient education resources, visit eMedicineHealth's Digestive Disorders Center
and Heart Health Center. Also, see eMedicineHealth's patient education articles Cirrhosis,
Hepatitis B, Hepatitis C, and Congestive Heart Failure.
Pathophysiology
The accumulation of ascitic fluid represents a state of total-body sodium and water excess,
but the event that initiates the unbalance is unclear. Three theories of ascites formation have
been proposed: underfilling, overflow, and peripheral arterial vasodilation.
The underfilling theory suggests that the primary abnormality is inappropriate sequestration
of fluid within the splanchnic vascular bed due to portal hypertension and a consequent
decrease in effective circulating blood volume. This activates the plasma renin, aldosterone,
and sympathetic nervous system, resulting in renal sodium and water retention.
The overflow theory suggests that the primary abnormality is inappropriate renal retention of
sodium and water in the absence of volume depletion. This theory was developed in
accordance with the observation that patients with cirrhosis have intravascular hypervolemia
rather than hypovolemia.
The most recent theory, the peripheral arterial vasodilation hypothesis, includes components
of both of the other theories. It suggests that portal hypertension leads to vasodilation, which
causes decreased effective arterial blood volume. As the natural history of the disease

3
progresses, neurohumoral excitation increases, more renal sodium is retained, and plasma
volume expands. This leads to overflow of fluid into the peritoneal cavity. The vasodilation
theory proposes that underfilling is operative early and overflow is operative late in the
natural history of cirrhosis.
Although the sequence of events that occurs between the development of portal hypertension
and renal sodium retention is not entirely clear, portal hypertension apparently leads to an
increase in nitric oxide levels. Nitric oxide mediates splanchnic and peripheral vasodilation.
Hepatic artery nitric oxide synthase activity is greater in patients with ascites than in those
without ascites.
Regardless of the initiating event, a number of factors contribute to the accumulation of fluid
in the abdominal cavity. Elevated levels of epinephrine and norepinephrine are well-
documented factors. Hypoalbuminemia and reduced plasma oncotic pressure favor the
extravasation of fluid from the plasma to the peritoneal fluid, and, thus, ascites is infrequent
in patients with cirrhosis unless both portal hypertension and hypoalbuminemia are present.
Epidemiology
Mortality/Morbidity
Ambulatory patients with an episode of cirrhotic ascites have a 3-year mortality rate of 50%.
The development of refractory ascites carries a poor prognosis, with a 1-year survival rate of
less than 50%.[1]
Sex
Healthy men have little or no intraperitoneal fluid, but women may normally have as much as
20 mL, depending on the phase of their menstrual cycle.
History
• Patients with ascites often state that they have recently noticed an increase in their
abdominal girth.
• Because most cases of ascites are due to liver disease, patients with ascites should be
asked about risk factors for liver disease. These include the following:
o Long-term heavy alcohol use
o Chronic viral hepatitis or jaundice
o Intravenous drug use
o Multiple sexual partners
o Homosexual activity with a male partner, or heterosexual activity with a
bisexual male
o Transfusion with blood not tested for hepatitis virus: in the United States,
screening of donated blood for hepatitis B virus (HBV) began in 1972; reliable
testing of the blood supply for hepatitis C virus (HCV) began in 1992 in
developed countries

4
 o Tattoos
o Living or birth in an area endemic for hepatitis
• Patients with alcoholic liver disease who alternate between heavy alcohol
consumption and abstention (or light consumption) may experience ascites in a cyclic
fashion.
• When a patient with a very long history of stable cirrhosis develops ascites, the
possibility of superimposed hepatocellular carcinoma (HCC) should be considered.
• Obesity, hypercholesterolemia, and type 2 diabetes mellitus are recognized causes of
nonalcoholic steatohepatitis, which can progress to cirrhosis.
• Patients with a history of cancer, especially gastrointestinal cancer, are at risk for
malignant ascites. Malignancy-related ascites is frequently painful, whereas cirrhotic
ascites is usually painless.
• Patients who develop ascites in the setting of established diabetes or nephrotic
syndrome may have nephrotic ascites.
Physical
The physical examination in a patient with ascites should focus on the signs of portal
hypertension and chronic liver disease.
• Physical findings suggestive of liver disease include jaundice, palmar erythema, and
spider angiomas.
• The liver may be difficult to palpate if a large amount of ascites is present, but if
palpable, the liver is often found to be enlarged. The puddle sign may be present when
as little as 120 mL of fluid is present. When peritoneal fluid exceeds 500 mL, ascites
may be demonstrated by the presence of shifting dullness or bulging flanks. A fluid-
wave sign is notoriously inaccurate.
• Elevated jugular venous pressure may suggest a cardiac origin of ascites. A firm
nodule in the umbilicus, the so-called Sister Mary Joseph nodule, is not common but
suggests peritoneal carcinomatosis originating from gastric, pancreatic, or hepatic
primary malignancy.
• A pathologic left-sided supraclavicular node (Virchow node) suggests the presence of
upper abdominal malignancy.
• Patients with cardiac disease or nephrotic syndrome may have anasarca.
Causes
• Normal peritoneum
o Portal hypertension (serum-ascites albumin gradient [SAAG] >1.1 g/dL)
▪ Hepatic congestion, congestive heart failure, constrictive pericarditis,
tricuspid insufficiency, Budd-Chiari syndrome

5
 ▪ Liver disease, cirrhosis, alcoholic hepatitis, fulminant hepatic failure,
massive hepatic metastases
o Hypoalbuminemia (SAAG < 1.1 g/dL)
▪ Nephrotic syndrome
▪ Protein-losing enteropathy
▪ Severe malnutrition with anasarca
o Miscellaneous conditions (SAAG < 1.1 g/dL)
▪ Chylous ascites
▪ Pancreatic ascites
▪ Bile ascites
▪ Nephrogenic ascites
▪ Urine ascites
▪ Ovarian disease
• Diseased peritoneum (SAAG < 1.1 g/dL)
o Infections
▪ Bacterial peritonitis
▪ Tuberculous peritonitis
▪ Fungal peritonitis
▪ Human immunodeficiency virus (HIV)-associated peritonitis
o Malignant conditions
▪ Peritoneal carcinomatosis
▪ Primary mesothelioma
▪ Pseudomyxoma peritonei
▪ Hepatocellular carcinoma
o Other rare conditions
▪ Familial Mediterranean fever
▪ Vasculitis
▪ Granulomatous peritonitis
▪ Eosinophilic peritonitis

6
Differential Diagnoses
• Acute Liver Failure
• Alcoholic Hepatitis
• Biliary Disease
• Budd-Chiari Syndrome
• Cardiomyopathy, Dilated
• Cardiomyopathy, Restrictive
• Cirrhosis
• Hepatitis, Viral
• Hepatocellular Adenoma
• Hepatorenal Syndrome
• Mediterranean Fever, Familial
• Nephrotic Syndrome
• Portal Hypertension
• Primary Biliary Cirrhosis
• Protein-Losing Enteropathy
Laboratory Studies
• In patients with new-onset ascites of unknown origin, peritoneal fluid should be sent
for cell count, albumin level, culture, total protein, Gram stain, and cytology.
o Inspection: Most ascitic fluid is transparent and tinged yellow. A minimum of
10,000 red blood cells/µL is required for ascitic fluid to appear pink, and more
than 20,000 red blood cells/µL will produce distinctly blood-tinged fluid. This
may result from either a traumatic tap or malignancy. Bloody fluid from a
traumatic tap is heterogeneously bloody, and the fluid will clot. Nontraumatic
bloody fluid is homogeneously red and does not clot because the blood has
already clotted and lysed. Cloudy ascitic fluid with a purulent consistency
indicates infection.
o Cell count: Normal ascitic fluid contains fewer than 500 leukocytes/µL and
fewer than 250 polymorphonuclear leukocytes (PMNs)/µL. Any inflammatory
condition can cause an elevated white blood cell count. A PMN count of

7
 greater than 250 cells/µL is highly suggestive of bacterial peritonitis.[2] In
tuberculous peritonitis and peritoneal carcinomatosis, lymphocytes usually
predominate.
o SAAG: The SAAG is the best single test for classifying ascites into portal
hypertensive (SAAG >1.1 g/dL) and non–portal hypertensive (SAAG < 1.1
g/dL) causes. Calculated by subtracting the ascitic fluid albumin value from
the serum albumin value, it correlates directly with portal pressure. The
specimens should be obtained relatively simultaneously. The accuracy of the
SAAG results is approximately 97% in classifying ascites. The terms high-
albumin gradient and low-albumin gradient should replace the terms
transudative and exudative in the description of ascites.
o Total protein: In the past, ascitic fluid has been classified as an exudate if the
protein level is greater than or equal to 2.5 g/dL. However, the accuracy is
only approximately 56% for detecting exudative causes. The total protein level
may provide additional clues when used with the SAAG. An elevated SAAG
and a high protein level are observed in most cases of ascites due to hepatic
congestion. The combination of a low SAAG and a high protein level is
characteristic of malignant ascites (see Causes).
o Culture/Gram stain: Culture has a 92% sensitivity for the detection of bacteria
in ascitic fluid, provided that samples are inoculated into blood culture bottles
immediately, at the bedside. In contrast, Gram stain is only 10% sensitive for
visualizing bacteria in early-detected spontaneous bacterial peritonitis.
Approximately 10,000 bacteria/mL are required for detection by Gram stain;
the median concentration of bacteria in spontaneous bacterial peritonitis is 1
organism/mL.
o Cytology: Cytology smears are reported to be 58-75% sensitive for detection
of malignant ascites.
Imaging Studies
• Chest and plain abdominal films
o Elevation of the diaphragm, with or without sympathetic pleural effusions
(hepatic hydrothorax), is visible in the presence of massive ascites. More than
500 mL of fluid is usually required for ascites to be diagnosed based on
findings from abdominal films.
o Many nonspecific signs suggest ascites, such as diffuse abdominal haziness,
bulging of the flanks, indistinct psoas margins, poor definition of the intra-
abdominal organs, erect position density increase, separation of small bowel
loops, and centralization of floating gas containing small bowel.
o The direct signs are more reliable and specific. In 80% of patients with ascites,
the lateral liver edge is medially displaced from the thoracoabdominal wall
(Hellmer sign). In the pelvis, fluid accumulates in the rectovesical pouch and
then spills into the paravesical fossa. The fluid produces symmetric densities
on both sides of the bladder, which is termed a "dog's ear" or "Mickey Mouse"

8
 appearance. Medial displacement of the cecum and ascending colon and
lateral displacement of the properitoneal fat line are present in more than 90%
of patients with significant ascites. Although obliteration of the hepatic angle
as been suggested as a sign of increased intra-abdominal fluid, this finding is
seen in 80% of healthy patients.

• Ultrasonography
o Real-time ultrasonography is the easiest and most sensitive technique for the
detection of ascitic fluid. Volumes as small as 5-10 mL can routinely be
visualized. Uncomplicated ascites appears as a homogeneous, freely mobile,
anechoic collection in the peritoneal cavity that demonstrates deep acoustic
enhancement. Free ascites does not displace organs but typically situates itself
between them, contouring to organ margins and demonstrating acute angles at
the point at which the fluid borders the organ.
o The smallest amounts of fluid tend to collect in the Morison pouch (posterior
subhepatic space) and around the liver as a sonolucent band. With massive
ascites, the small bowel loops have a characteristic polycyclic, "lollipop," or
arcuate appearance because they are arrayed on either side of the vertically
floating mesentery.
o Certain ultrasonographic findings suggest that the ascites may be infected,
inflammatory, or malignant. These findings include coarse internal echoes
(blood), fine internal echoes (chyle), multiple septa (tuberculous peritonitis,
pseudomyxoma peritonei), loculation or atypical fluid distribution, matting or
clumping of bowel loops, and thickening of interfaces between fluid and
adjacent structures. In malignant ascites, the bowel loops do not float freely
but may be tethered along the posterior abdominal wall, plastered to the liver
or other organs, or surrounded by loculated fluid collections.
o Most patients (95%) with carcinomatous peritonitis have a gallbladder wall
that is less than 3 mm thick. Mural thickening of the gallbladder is associated
with benign ascites in 82% of cases. The thickening of the gallbladder is
primarily a reflection of cirrhosis and portal hypertension.
• Computed tomography (CT) scanning: Ascites is demonstrated well on CT scan
images. Small amounts of ascitic fluid localize in the right perihepatic space, the
posterior subhepatic space, and the Douglas pouch (rectouterine pouch). See the

image below. This computed tomography scan

demonstrates free intraperitoneal fluid due to urinary ascites.

9
 o A number of CT scan features suggest neoplasia. Hepatic, adrenal, splenic, or
lymph node lesions associated with masses arising from the gut, ovary, or
pancreas are suggestive of malignant ascites. Patients with malignant ascites
tend to have proportional fluid collections in the greater and lesser sacs;
whereas, in patients with benign ascites, the fluid is observed primarily in the
greater sac and not in the lesser omental bursae.
Other Tests
• Laparoscopy may be valuable for the diagnosis of otherwise unexplained cases,
especially if malignant ascites is suspected. This may be of particular importance in
the diagnosis of malignant mesothelioma.
Procedures
Abdominal paracentesis: Abdominal paracentesis is the most rapid and perhaps the most cost-
effective method of diagnosing the cause of ascites formation. Guidelines from the American
Association for the Study of Liver Diseases (AASLD) for management of adult patients with
ascites due to cirrhosis advocate paracentesis in all patients with clinically apparent new-
onset ascites (grade II-3 recommendation).
Bleeding from paracentesis is sufficiently uncommon that the AASLD does not recommend
the prophylactic use of fresh frozen plasma or platelets beforehand (grade III).
For more detailed information regarding paracentesis, including images and video, please see
the Medscape article Paracentesis [in the Clinical Procedures section].
Staging
• Ascites may be semi-quantified using the following system:
o Stage 1+ is detectable only after careful examination.
o Stage 2+ is easily detectable but of relatively small volume.
o Stage 3+ is obvious, but not tense, ascites.
o Stage 4+ is tense ascites.
Medical Care
Sodium restriction (20-30 mEq/d) and diuretic therapy constitute the standard medical
management for ascites and are effective in approximately 95% of patients.
• Water restriction is used only if persistent hyponatremia is present (see Diet, below).
• Recent research has focused on the treatment of refractory ascites with aquaretics—
vasopressin V2-receptor antagonists that promote excretion of electrolyte-free water
and thus might be beneficial in patients with ascites and hyponatremia. Although
study results have been promising, aquaretics still await approval by the Food and
Drug Administration (FDA).
• Therapeutic paracentesis may be performed in patients who require rapid
symptomatic relief for refractory or tense ascites. When small volumes of ascitic fluid

10
 are removed, saline alone is an effective plasma expander. The removal of 5 L of fluid
or more is considered large-volume paracentesis. Total paracentesis, that is, removal
of all ascites (even >20 L), can usually be performed safely. Supplementing 5 g of
albumin per each liter over 5 L of ascitic fluid removed decreases complications of
paracentesis, such as electrolyte imbalances and increases in serum creatinine levels
secondary to large shifts of intravascular volume. Note: The AASLD indicates that
postparacentesis albumin infusion may not be necessary for a single paracentesis of
less than 4 to 5 L; however, for large-volume paracenteses, the AASLD suggests
considering an albumin infusion of 8-10 g per liter of fluid removed (Grade II-2).
• To avoid exposing patients to blood products, the use of terlipressin (eg, 1 mg every 4
hours for 48 hours) rather than albumin has been proposed for prevention of
circulatory dysfunction after large-volume paracentesis. Initial studies suggest that
terlipressin is as effective as albumin for this purpose.
• Repeated therapeutic paracentesis can be used to treat refractory ascites. For palliative
care in patients with advanced cancer, an alternative to serial paracenteses is
placement of an indwelling peritoneal catheter; ascitic fluid can then be removed by
continuous drainage or intermittent drainage with a proprietary system utilizing
vacuum bottles, which can be performed in the patient’s home. Preservation of good
nutrition status is important.
• The transjugular intrahepatic portosystemic shunt (TIPS) is an interventional
radiologic technique that reduces portal pressure and may be the most effective
treatment for patients with diuretic-resistant ascites. In the procedure, which is
performed with the patient under conscious sedation or general anesthesia, an
interventional radiologist places a stent percutaneously from the right jugular vein
into the hepatic vein, thereby creating a connection between the portal and systemic
circulations. TIPS is gradually becoming the standard of care in patients with diuretic-
refractory ascites.
Surgical Care
The peritoneovenous shunt is an alternative for patients with medically intractable ascites
(see image below).

Peritoneovenous shunt.
This is a megalymphatic shunt that returns the ascitic fluid to the central venous system.
Beneficial effects of these shunts include increased cardiac output, renal blood flow,
glomerular filtration rate, urinary volume, and sodium excretion and decreased plasma renin

11
activity and plasma aldosterone concentration. Although it has largely been supplanted by
TIPS, peritoneovenous shunting has been shown to improve short-term survival (compared
with paracentesis) in cancer patients with refractory malignant ascites. The AASLD suggests
considering peritoneovenous shunting for patients with refractory ascites who are not
candidates for paracentesis or TIPS (Grade I).
The AASLD (American Assoc for the Study of Liver Disease) recommends that patients with
cirrhosis and ascites be considered for liver transplantation.
Consultations
Consultation with a gastrointestinal specialist and/or hepatologist should be considered for all
patients with ascites, particularly if the ascites is refractory to medical treatment.
Diet
Sodium restriction of 500 mg/d (22 mmol/d) is feasible in a hospital setting; however, it is
unrealistic in most outpatient settings. A more appropriate sodium restriction is 2000 mg/d
(88 mmol). Indiscriminate fluid restriction is inappropriate. Fluids need not be restricted
unless the serum sodium level drops below 120 mmol/L.

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications in
patients with ascites.
Diuretics
Class Summary
Diuretic agents are the mainstay of medical therapy in ascites.
Spironolactone (Aldactone)
For the management of edema resulting from excessive aldosterone excretion. Competes with
aldosterone for receptor sites in distal renal tubules, increasing water excretion while
retaining potassium and hydrogen ions. The peak effect of Aldactone is approximately 3 d.
Furosemide (Lasix)

Increases the excretion of water by interfering with chloride-binding cotransport system,

which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and
distal renal tubule. Dose must be individualized to patient.
Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after
the previous dose, until the desired diuresis occurs. When treating infants, titrate in
increments of 1 mg/kg/dose until a satisfactory effect is achieved.

Amiloride (Midamor)

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A pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic
agents. Potassium-conserving (antikaliuretic) drug which, compared with thiazide diuretics,
possesses weak natriuretic, diuretic, and antihypertensive activity.
Metolazone (Mykrox, Zaroxolyn)
Helps treat edema in congestive heart failure. Increases excretion of sodium, water,
potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. May be
more effective in those with impaired renal function.
Mannitol (Osmitrol)
Inhibits tubular reabsorption of electrolytes by increasing the osmotic pressure of glomerular
filtrate. Increases urinary output.
Further Inpatient Care
• Patients can actually be maintained free of ascites if sodium intake is limited to 10
mmol/d. However, this is not practical outside a metabolic ward.
• Twenty-four – hour urinary sodium measurements are useful in patients with ascites
related to portal hypertension in order to assess the degree of sodium avidity, monitor
the response to diuretics, and assess compliance with diet.
• For grade 3 or 4 ascites, therapeutic paracentesis may be necessary intermittently.
Further Outpatient Care
• The best method of assessing the effectiveness of diuretic therapy is by monitoring
body weight and urinary sodium levels.
• In general, the goal of diuretic treatment of ascites should be to achieve a weight loss
of 300-500 g/d in patients without edema and 800-1000 g/d in patients with edema.
• Once ascites has disappeared, diuretic treatment should be adjusted to maintain the
patient free of ascites.
Inpatient & Outpatient Medications
• Diuretics should be initiated in patients whose ascites does not respond to sodium
restriction. A useful regimen is to start with spironolactone at 100 mg/d. The addition
of loop diuretics may be necessary in some cases to increase the natriuretic effect. If
no response occurs after 4-5 days, the dosage may be increased stepwise up to
spironolactone at 400 mg/d plus furosemide at 160 mg/d.
Complications
• The most common complication of ascites is the development of spontaneous
bacterial peritonitis (ascitic fluid with PMN count of >250 μ L).
o Performing repeated physical examinations and paying particular attention to
abdominal tenderness may be the best way to become aware of the possible
development of this complication. In a study of 133 hospitalized patients with

13
 ascites, abdominal pain and abdominal tenderness were more common in
patients with spontaneous bacterial peritonitis (P < 0.01), but no other physical
sign or laboratory test could separate spontaneous bacterial peritonitis cases
from other cases.
o Any patient with ascites and fever should have a paracentesis with bedside
blood culture inoculation and cell count. Patients with a protein level of less
than 1 g/dL in ascitic fluid are at high risk for the development of spontaneous
bacterial peritonitis. Prophylactic antibiotic therapy with a quinolone is often
recommended.
• Complications of paracentesis include infection, electrolyte imbalances, bleeding, and
bowel perforation. Bowel perforation should be considered in any patient with recent
paracentesis who develops a new onset of fever and/or abdominal pain. All patients
with long-standing ascites are at risk of developing umbilical hernias. Large-volume
paracentesis often results in large intravascular fluid shifts. This can be avoided by
administering albumin replacement if more than 5 L is removed.
Prognosis
• The prognosis for patients with ascites due to liver disease depends on the underlying
disorder, the degree of reversibility of a given disease process, and the response to
treatment.
Patient Education
• The most important aspect of patient education is determining when therapy is failing
and recognizing the need to see a physician. Unfortunately, in most cases, liver failure
has a dismal prognosis. All patients must be taught which complications are
potentially fatal and the signs and symptoms that precede them.
Abdominal distention and/or pain despite maximal diuretic therapy are common problems,
and patients must realize the importance of seeing a physician immediately

14
 CASES
REAL CASE

A) Patient History
Real case I studied is recurrent ascites secondary to liver disease. Patient name, Kamarul Bin
Adli (RN 7346), aged 64 years old, came to Emergency department of Hospital Slim River
accompanied by his wife with the chief complaint of shortness of breath for 2 days ago. The
history of presenting complaint made by the patient is cough for 2 days, abdominal distension
for 2 weeks and breathing difficulty for 1 week. This patient has past medical history,
diagnosed on medications and regular follow up at Klinik Kesihatan Tanjung Malim,hepatitis
C since year 2015, chronic liver disease since year 2017, this medical history diagnosed on
medications and regular follow up at Klinik Pakar Medikal, Hospital slim River and this patient
also do not have any surgical history.

FAMILY TREE
Wife Patient
-59 years old -64 years old
- hepatitis C, chronic liver
disease,

1st 2nd
son daughter
3rd Daughter
38 years old 32 years old 27 years old

15
Based on patient’s family history, we know that this patient’s wife also has medical history of
diabetes mellitus and hypertension and have 3 children. This patient does not have any drug
allergic. While according to social history, we get to know this patient is a retired fireworker,
non-alcoholic and non smoking person.

B) Physical examination

During general examinations, this patient is look alert, conscious which achieve 15/15 Glasgow
coma scale (GCS), pale, have good pulse volume and have a good hydration. His vital signs
are observed and recorded.

The vital sign of this patient is,

Vital Sign On arrival Current

Blood pressure (BP) 120/76 mmHg 128/77 mmHg
Pulse rate (PR) 91 bpm 84 bpm
Respiration rate (RR) 24/min 21/min
Body temperature (BT) 37.8 degree Celsius 37.1 degree Celsius
Spo2 98 % under room air 100 % under nasal prong
DXT 10.8 -

Cardiovascular system is shows systolic murmur at left sternal edge. When auscultate the lungs,
air entry reduced bilaterally and crepitation at base of lungs. While during palpitation,
abdominal distension ascites was detected.

Other physical examination found in her body is fluid accumulation of abdominal.

16
 Fluid trapped,bowel
dullness

C) Differential diagnosis

- Fluid overload secondary to non-compliance to restriction of fluid (ROF)

- Cellulitis

- Congestive cardiac failure on restriction of fluid

- Pneumonia

- Pulmonary embolism

D) Investigation

After undergoing the history of patient, physical examination and finding differential
diagnosis, next doctor carries out some laboratory and radiology investigation. For laboratory
test, full blood count (FBC) were taken. The result is as shown below:

Full blood count Result Normal range

White blood count (WBC) 8.84 x10^3/UL 4.0-10.0

Total red cells 3.33 x10^6/UL 4.5-5.5

Haemoglobin 9.7 g/dl 13-18
Platelet count 104 x 10^3/UL 150-450
HCT 28.9 % 40-50
Next the result of liver function test is as shown below:

Liver function test Result Normal range

Total protein 68.9 g/L 60- 80

Albumin 14.6 g/L 35-52

17
 Globulin 54.3 g/L 18- 36
Total bilirubin color 34.4 umol/L 3.4- 17
Alkaline phosphatase 163 U/L 34- 120
Aspartate Amino 94.6 U/L 9.0- 48.0
Transaminase
Alanine Amino 43.3 U/L 5.0- 49.0
Transferase
A/G Ratio 0.3 0.9- 1.8
While the result for renal profile (RP) is as shown below:

Renal profile Result Normal range

Blood urea nitrogen 10.2 mmol/L 1.7-8.3
Sodium 128.3 mmol/L 135-154
Potassium 3.6 mmol/L 3.6-5.4
Chloride 97.7 mmol/L 93-108
Creatinine 118 umol/L 48-95

Next laboratory test used by doctors in my case is INR which shows the result 1.36.

Urine FEME also shows the result as shown below:

Urine FEME Result

Leucocyte 1+
Nitrite Negative
Urobilinogen 1+
pH 5.0
Protein Negative
Blood 3+
Specific gravity 1.020
Ketones +/-
Bilirubin Negative
Glucose Negative

18
Beside this laboratory investigations, doctor carry out other radiology tests like
electrocardiogram (ECG), chest x-ray shows fluid in the base of lungs and blood glucose test
(DXT) shows 10.8 mmol.

E) Diagnosis

Recurrent ascites with underlined chronic liver disease.

F) Treatment and management

Initial Management

Patient came to emergency department accompanied by his wife due to shortness of breath for
3 days. Patient is referred from Klinik Kesihatan Tanjung Malim. Next, assistant medical
officer was checking for the patients’ vital sign and monitoring electrocardiogram. Next initial
management done in secondary triage was triage this patient to yellow zone. Before triage this
patient, assistant medical officer in charged was took patient’s t history, including family, drug
and social history.

Routine Management

- Doing bed making before patient arrive to yellow zone

- Checking for the patient’s vital sign per hourly
- Provide nursing care and patient rest in bed
- Insert branula and observe branula intact to avoid from occurring bleeding
- Give medication to patient based on doctor’s order
- Chest x-ray of patient were taken
- Strict input and output (I/O) chart
Specific Management

- Patient transfer from yellow to red zone

- Insert catheter bladder drainage (CBD) bag to patient after arriving to red zone
- Given CPAP to the patient to give positive pressure into the lungs and remove excessive
of fluid in pleural space
- Later given 5 litre nasal prong oxygen
- Take blood glucose test (DXT) 4 hourly
- Patient refer to medical department for further management
- Doctor in medical department plan to admit this patient to ward 10

19
 - Medical doctor who is in charged was asked the patient to bring old notes and old
medicine to ward 10
- Peritoneal tapping was done to this patient
- Once again take blood and chest x-ray test
- ABG (arterial blood gas) test was took in red zone

Treatment

Pharmacological treatment

Drugs Generic name Trade name Dose Indication

IV Ranitidine Ranitidine ZANTAC 1.ADULT: Slow 1.Benign
50 mg stat 25mg/ml injection Injection IV injection of 50 gastric/
mg diluted to 20 duodenal
ml and given over ulceration,
at least 2 minutes. reflux
May be repeated oesophagitis,
every 6-8 hours Zollinger Elliso
or IV infusion at syndrome
rate of 25 2. stress ulcer
mg/hour for 2 prophylaxis in
hours, may be post-operative
repeated at 6-8 and high risk
hours intervals or patient
IM. CHILD: 1
mg/kg/dose 6-8
hourly.
2.Initial slow IV
injection of 50
mg, then
continuous
infusion of 125-
250mcg/ kg/hour

20
IV Lasix 40mg Frusemide LASIX Initially 20-40 Pulmonary
Stat/IV 10mg/ml injection injection mg IM or slow IV edema
Frusemide (rate not
40mg TDS exceeding
4mg/min).
CHILD: 0.5-1.5
mg/kg. Max:
20mg daily.
Human Albunorm The infusion rate Restoration and
Albumin 20% infusion should be maintenance of
20g/ml 20g/ml adjusted circulating
according to the blood volume
individual
circumstances
and the
indication.in
plasma exchange
the infusion rate
should be
adjusted

G) Advice
• Ask patient to follow up at Klinik Pakar Medical, Hospital Slim River
• Eat medications followed by the dosage that had been prescribed by doctor
• Do simple exercise
• Take plenty of rest
• Drink water according to doctors’ order
• Eat healthy and vitamin rich diet
• Avoid stress
• Follow salt restriction
• Avoid harmful environment factor such as smoke or dust and chemical
• Take care personal hygiene to avoid from infection

21
REFERENCE A
Background Malignant ascites is the accumulation of abdominal fluid due to the direct
effects of cancer. This causes and diagnosis of malignant ascites will review its treatment.
Pathophysiology The pathophysiology of malignant ascites is incompletely understood.
Contributing mechanisms include tumor-related obstruction of lymphatic drainage, increased
vascular permeability, over-activation of the renin-angiotensin-aldosterone system, neoplastic
fluid production, and production of metalloproteinases that degrade the extracellular matrix.
Portal venous compression can also occur from metastatic invasion of the liver, leading to
peritoneal fluid accumulation.
Natural History The most common cancers associated with ascites are adenocarcinomas of
the ovary, breast, colon, stomach and pancreas. Median survival after diagnosis of malignant
ascites is in the range of 1-4 months; survival is apt to be longer for ovarian and breast
cancers if systemic anti-cancer treatments are available.
Presentation and Diagnostics Symptoms include abdominal distension, nausea, vomiting,
early satiety, dyspnea, lower extremity edema, weight gain, and reduced mobility. Physical
exam findings may include abdominal distention, bulging flanks, shifting dullness, and a
fluid wave. Plain abdominal x-rays are not specific, but may show a hazy or a “ground glass”
appearance. Ultrasound or CT scanning can confirm the presence of ascites and also
demonstrate if the fluid is loculated in discrete areas of the peritoneal cavity.
There are many potential causes of ascites in the cancer patient: peritoneal carcinomatosis,
malignant obstruction of draining lymphatics, portal vein thrombosis, elevated portal venous
pressure from cirrhosis, congestive heart failure, constrictive pericarditis, nephrotic
syndrome, and peritoneal infections.
Depending on the clinical presentation and expected survival, a diagnostic evaluation is
usually indicated as it will impact both prognosis and treatment approach. Key tests include
the serum albumin and protein level and a simultaneous diagnostic paracentesis, checking
ascitic fluid white blood cell count, albumin, protein, and cytology.
Classification The old classification of exudative versus transudative ascites has been
updated through the use of the serum-ascites albumin gradient (SAAG).
SAAG = (the serum albumin concentration) – (ascitic fluid albumin concentration).
A SAAG > 1.1 g/dl indicates ascites due to, at least in part, increased portal pressures, with
an accuracy of 97%. This is most commonly seen in patients with cirrhosis, hepatic
congestion, CHF, or portal vein thrombosis.
A SAAG < 1.1 g/dl indicates no portal hypertension, with an accuracy of 97%; most
commonly seen in peritoneal carcinomatosis, an infectious process of the peritoneum,
nephrotic syndrome, or malnutrition/hypoalbuminemia.
Cytological evaluation is approximately 97% sensitive in cases of peritoneal carcinomatosis,
but is not helpful in the detection of other types of malignant ascites due to massive hepatic
metastasis or malignant obstruction of lymph vessels.

22
Introduction
Malignant ascites is the abnormal accumulation of fluid in the peritoneal cavity associated
with several intrapelvic and intra-abdominal malignancies. When occurring in a setting other
than ovarian cancer, malignant ascites is associated with a poor prognosis1 and impacts the
remaining days of patients lives by contributing to symptom burden, causes frequent and
unnecessary hospitalization, and leads to poor quality of life.2 Palliative options that have
been used for malignant ascites have included fluid restriction, diuretics, peritoneal-venous
shunts, and most recently the Food and Drug Administration (FDA) approved PleurX®
catheter.3 Most of these therapies are not uniformly successful or are associated with adverse
effects which limit their use. More options are needed for palliation. The development of
monoclonal technologies as well as advances in basic science cancer research have identified
potential targets for monoclonal therapies and have initiated the use of monoclonal therapies
for the treatment of malignant ascites. Catumaxomab4 represents a new advance in the
management of malignant effusions. A trifunctional molecule, this monoclonal antibody
targets overexpressed epithelial markers associated with malignancies which are commonly
associated with malignant ascites, and harnesses the immune system to target the immune-
mediated destruction of tumor cells causing ascites. This article reviews relevant therapies for
malignant ascites and also illustrates how new therapies such as catumaxomab may play a
role in the palliation of malignant ascites.
Go to:
Epidemiology
The malignancies most commonly associated with malignant ascites include the gynecologic
malignancies, gastrointestinal malignancies, as well as breast cancer and carcinoma of
unknown primary. Among the gynecologic malignancies, ovarian carcinoma predominates.
Of the gastrointestinal malignancies, ascites can occur with advanced colon, pancreas, gastric
carcinoma, and esophageal carcinoma. One retrospective review5 of causes of malignant
ascites found that ovarian cancer had the highest proportion of patients who developed ascites
at 37.7%, followed by pancreaticobiliary cancers (21%), gastric cancer (18.3%), esophageal
cancer (4.0%), colorectal cancer (3.7%), and breast cancer (3.0%). This particular series had
a low incidence of ascites associated with hepatocellular carcinoma. The study also found
that the number of cases of malignant ascites due to an unknown primary cancer was only
8.1% compared to previous reports. Previous estimates also suggest that up to 20% of cases
of carcinoma of unknown primary have been associated with ascites.5 Advances in imaging
and immunocytochemical analysis, with the result being better tumor identification, will
continue to influence a decline in the number of cases of malignant ascites associated with
carcinoma of unknown primary.
Go to:
Pathophysiology
While the pathophysiology of malignant ascites is not totally understood, factors that
contribute to the development of ascites include lymphatic obstruction by tumor cells, excess
vascular permeability, and hormonal effects, as well as other tumor-specific effects such as
excess metalloproteinase production.6 The ability of positive cytology to obstruct draining
catheters testifies to the potential effect of tumor cells on smaller lymphatic channels.

23
Increases in vascular permeability have received much attention as factors causing malignant
ascites. In particular, vascular endothelial growth factor (VEGF) has not only been implicated
as a factor for tumor growth, but VEGF has also been cited as an important factor affecting
vascular permeability, a key factor in ascites production.7 VEGF is a potent growth factor
that stimulates blood vessel formation as well as exerting effects on the vascular endothelial
cell. A potent permeability factor, it is 50,000 times as potent as histamine.8 VEGF plays a
role in the pathophysiology of malignant ascites with malignant cells overexpressing VEGF
and producing high levels in ascitic fluid.9 High levels of VEGF are found in the malignant
effusions of ovarian, colorectal, and breast cancer patients.9 In preclinical models, the
administration of malignant ascitic fluid to animals without malignant ascites can cause
malignant ascites.10 Blockade of VEGF with a monoclonal antibody can reverse the severity
of ascites in animal models.11 VEGF levels respond to therapy and are lowered with
chemotherapy treatments of malignancy.12 Hormonal mechanisms have been implicated and
may play a role in the development of ascites as some cases of malignancy associated ascites
respond to diuretics, in particular those cases with elevated renin levels.13 Matrix
metalloproteinases are also postulated to influence the development of malignant ascites.
They degrade the extracellular matrix and facilitate the spread of tumors, undoubtedly
contributing to tumor-related increases in permeability. Inhibitors of metalloproteinases can
cause formation of ascites.14
Go to:
Symptoms
Ascites can cause significant symptoms referable to the gastrointestinal and genitourinary
tract. Common gastrointestinal symptoms include distension, nausea, and vomiting. Patients
experience dyspnea, as well as weight gain and edema. One survey15 of symptoms from
women with ovarian cancer describe bloating, swelling, fatigue, urinary frequency,
constipation, abdominal and pelvic pain, back pain, anorexia, and vaginal bleeding, as well as
gastrointestinal symptoms such as indigestion, constipation, abdominal cramping, diarrhea,
gas, or movement in pelvis.
Go to:
Evaluation
Evaluation consists of physical examination and radiographic imaging. Important clues as to
the etiology of ascites come from analysis of the fluid itself.
Physical examination
Physical examination is not reliable for the diagnosis of ascites, especially in obese patients.
Maneuvers used to detect ascites include testing for flank dullness, which if present is a
reliable physical sign of ascites. Flank dullness, though, requires the presence of at least 1500
cc of fluid to be present for flank dullness to be detected. Overall, physical exam has less than
optimal sensitivity and specificity.16
Imaging
Ultrasound

24
Ultrasound is one of the quickest screening tests for the detection of ascites. Ultrasound may
detect as little as 100 cc of ascitic fluid.17
Computerized tomography
Computerized tomography can also detect ascites and also plays an important role for the
cancer patient by providing an estimate of overall disease burden, and is capable of
determination of disease progression.18 The determination of disease progression may
influence approaches to the management of malignant ascites.
Plain films
Plain films show a ground glass appearance and can suggest the presence of ascites.
Go to:
Ascitic fluid analysis
Visual inspection
Gross observation of the fluid can provide some clues to the etiology of ascites. Grossly
bloody fluid is consistent with malignancy.18 Bleeding in the peritoneal cavity can be seen
with hepatocellular carcinoma.19 Cloudy fluid suggests infection. Milky fluid suggests
chylous ascites.20 Chylous ascites has a trigylceride content of >200 mg/dL. Chylous ascites
is often associated with malignancy, especially lymphoma.
Chemical analysis of ascitic fluid
Dividing ascitic fluid into the transudate and exudate categories, such as is done with
malignant pleural effusions using lactate dehydrogenase (LDH), protein and the ratios of
these values (serum to ascites) has not proven to be beneficial for malignant ascites. One test
of the fluid that has been useful for distinguishing malignant from cirrhotic causes of ascites
is the serum-to-ascites albumin gradient.
Serum to ascites albumin gradient
The serum-to-ascites albumin gradient is especially useful when the etiology of ascites is in
doubt, such as in the case of a patient with new onset ascites, or new ascites that occurs in the
setting of liver cirrhosis. A gradient greater than or equal to 1.1 g/dL indicates portal
hypertension with 97% accuracy, whereas a lower gradient (high-protein ascites) indicates a
lack of portal hypertension and possibly the presence of a malignancy.21
Cytology
The presence of malignant cells in the ascitic fluid confirms the diagnosis of malignancy with
a specificity of 100% and is the gold standard for the diagnosis. Cellular content of ascitic
fluid represents shedding of tumor cells from the tumor into the peritoneal fluid. The yield of
cytology is greater with primary peritoneal tumors.19 The sensitivity of cytology is only
60%, as not all tumors shed cells into the peritoneum.22
Immunohistochemistry

25
Immunochemistry can help distinguish cancer cells from nonmalignant cells such as
mesenchymal cells.23 Immuno-histochemical techniques have not replaced cytology as the
gold standard for the diagnosis of malignant ascites.
Go to:
Prognosis
The presence of malignant ascites has a strong negative prognostic import; however, there are
differences in prognosis when individual malignancies are considered. One retrospective
study reviewed experience with malignant ascites over 10 years.5 The gastrointestinal
malignancies associated with the poorest prognosis were gastric carcinoma (associated with a
median survival of 1.4 months), colon cancer (with a median survival of 3.7 months), and
pancreatic cancer (with a median survival of 1.4 months). The study found that ascites of
ovarian origin has a better median survival than all other cancer groups, which is in
agreement with previous studies.13 In addition to origin of malignancy as being
prognostically important, other factors such as low serum albumin, can be independent
prognostic factors, especially in the nonovarian cancer groups.24 Other factors important in
prognosis of malignant ascites in nonovarian cancer groups include liver metastases, and
elevated serum bilirubin.25
Go to:
Management
Symptomatic management by paracentesis
Paracentesis can result in rapid symptom control in 90% of patients.26 One major concern is
how much and how fast fluid can be removed. There is no agreement on the optimal rate of
fluid removal, with no reports of increased adverse effects associated with a rapid rate of
paracentesis. Concern exists that large volume fluid removal may lead to renal impairment
and hypotension. In response to these concerns, which are well documented in the
nonmalignant liver disease population, two studies have suggested that large volume
paracentesis in malignant ascites can be performed without complication. In both studies,
large volumes of ascitic fluid were removed without the routine need for correction of
hypovolemia.27,28 Paracentesis can be done safely in the presence of coagulopathy.29 There
is no evidence for benefit with the use of albumin infusions for patients with malignant
ascites as a means of maintaining intravascular volume after large volume paracentesis.30
Complications of paracentesis
Besides concerns about hypovolemia after large volume paracentesis, other concerns are for
infection and rarely, pulmonary embolization.31 There is a risk of hypoalbuminemia with
repeated paracentesis.32
Diuretics
There is a lack of randomized trials to assess the efficacy of diuretics in malignant ascites.33
Uncontrolled trials show an average response rate of 44% when diuretics are used in
malignant ascites.34–37 Responses have been identified in those with increased renin values,
as well as elevated serum-ascites albumin gradient (SAAG) suggesting a likely response

26
when there are characteristics of nonmalignant liver disease present, which can occur in
patients with malignant ascites.
Peritoneal-venous shunting
Shunts function as a connection between the peritoneal cavity and large venous vessels, such
as the vena cava, allowing escape of the peritoneal fluid back into the circulation. Two types
of shunts are available, the LeVeen and the Denver shunt.38 Both shunts direct ascitic fluid
into the vena cava through a one-way valve. Higher pressures to achieve increased flow are
achievable with the LeVeen shunt. Both types of shunts were designed to prevent repeated
paracentesis and prevent protein loss that can occur with repeated paracentesis.37 Shunts
palliate symptoms in 70% of patients.37,39–41 Complications associated with shunt
placement include disseminated intravascular coagulation, postoperative pulmonary edema,
fever, and infection.42 Shunting is contraindicated in patients with fulminant hepatic failure
and active disseminated intravascular coagulation (DIC).42 Shunting is relatively
contraindicated in patients with positive cytology.42 Shunt block occurs more often in the
patients with positive cytology and the shunt tends to function longer in the patient with
cytologically negative fluid.42 The median shunt survival in patients with negative cytology
was 140 days compared with 26 days in the positive group.42 High ascitic fluid protein and
hemorrhagic effusions also lead to increased risk for shunt block.42 The overall incidence of
shunt block is approximately 2%. Volume overload occurs in 10%–16% of cases. Another
unproven concern is the dissemination of tumor cells throughout the body.3 The implication
is that the disease can be worsened, as the patients for whom this procedure is used have
advanced disease by virtue of having malignant ascites. Fever is another complication that
must be distinguished from active infection. True fever associated with shunting is
transient.43 There have been no successful studies comparing the superiority of one shunt
type over the other in malignant ascites. Parsons and associates demonstrated no survival or
quality-of-life advantage when peritoneovenous shunting was compared with repeated
paracentesis.24 Shunts may not be an optimal option in patients with gastrointestinal
malignancies, as the response rates for symptom control are inferior to those with shunts
associated with malignant ascites and ovarian and breast cancer.13,44
Catheter drainage
Catheter drainage remains an important option for the patient with malignant ascites.
Advantages include easy drainage, and patient self-drainage.45 Catheters eliminate frequent
trips to the hospital, the avoidance of procedural discomfort from repeated paracentesis, and
enhance autonomy for the patient. Concerns about catheter drainage have included infection,
protein loss, and technical complications such as catheter dislodgment and blockage. Types
of catheters include the simple catheter, tunneled catheters, percutaneously placed peritoneal
ports, modified venous access ports, and the PleurX catheter.46 The PleurX catheter was
FDA approved for the management of malignant ascites in 2005.47 There have been no
comparisons of one catheter type versus another. Whatever the method of drainage, large
volume paracentesis (>500 cc) can be done. Infection risk with the use of drainage catheters
is complicated by small numbers of published data and lack of comparisons between catheter
types.46 Peritonitis has been associated with catheter use, but it is unclear if peritonitis is
directly related to catheter insertion. There is no data regarding superiority of one catheter
type versus another with regards to incidence of dislodgement, leakage, blockage, or

27
infection. Noncuffed catheters may be associated with a higher infection rate.46 The
incidence of infection with drainage catheters, such as the PleurX catheter, has been a cause
for concern. A recent retrospective review of the literature found that in 221 ± 19 patients
with malignant ascites requiring catheter placement, a higher incidence of infection was
associated with untunneled catheters.2,46 Estimates of infection rates with untunneled
catheters are approximately 11%.2 There is no data as to the exact degree of protein loss that
occurs with catheter drainage, and whether or not that catheter-related protein loss is
associated with worsening symptoms. There is no opinion on how loculation of peritoneal
fluid affects performance of catheter placement or its success.
Go to:
New approaches to malignant ascites
Octreotide
Octreotide, a somatostatin analog given for the management of malignant bowel obstruction,
acts as an antisecretory agent and was found in a case series to successfully reduce ascites.48
This has not been evaluated further.
Anti-VEGF therapy
The use of inhibitors of the tyrosine kinase activity of VEGF has been shown to inhibit
formation of ascites in cell lines and animal models.49,50 Unfortunately there have been are
no human studies at this time with this modality.
Go to:
Metalloproteinase inhibitors
Human studies have been conducted with metalloproteinase inhibitors such as batimastat.51
In a phase I study, 22 patients with malignant ascites (16 patients with ovarian cancer, two
patients with sarcoma, one patient with breast cancer, one patient with renal carcinoma, one
patient with colon cancer, and one patient with endometrial cancer) had batimastat instilled
into the peritoneal cavity after paracentesis. No reaccumulation of ascites occurred after that
single dose in five of the 23 patients, and these five survived for up to 112 days. Seven other
patients died without reaccumulation during this follow-up period. The major adverse effect
in the first 24 hours was nausea and vomiting.
Go to:
Immunologic therapies
Intraperitoneal immunotherapy Interferon
Immunotherapy, via activation of patients’ cellular immunity, has been used in ovarian
carcinoma for the treatment of malignant ascites. Intraperitoneal interferon is capable of
stopping ascitic fluid production in ovarian cancer. One small study52 of 10 patients showed
resolution of ascites in 3/10 when interferon is given intraperitoneally to patients with ovarian
cancer. Parenteral interferon was studied in five patients, with 2/5 having cessation of ascitic
fluid production.53

28
Tumor necrosis factor-α
Tumor necrosis factor-α (TNF-α) has also been reported to be an effective palliative
treatment for malignant ascites.54 In that study of 29 patients with refractory malignant
ascites (10 with ovarian cancer, two with breast cancer, five with colorectal cancer, six with
gastric cancer, four with pancreatic cancer, one with hepatic cancer, and one with endometrial
cancer), 22 responded to intraperitoneal TNF-α administration. Of these 22, 16 had complete
and six had partial resolution of their ascites. The response seemed to predominate in patients
with nonbulky distribution of tumor in the abdomen. Adverse effects of fever, chills, nausea,
vomiting, and fatigue were reported, but these were generally well tolerated.
New immunologic approaches: new targets
New therapeutic approaches to the management of malignant ascites have taken advantage of
new basic science about cancer cells and advances in the technology of monoclonal antibody
therapy. One important discovery is that cellular adhesion molecules are overexpressed in
several malignancies and thus have become a target for the advanced monoclonal antibody
technology. One cellular adhesion protein called epithelial cell adhesion molecule (EpCAM)
is a 40 kDa cell surface glycoprotein that mediates epithelium-specific, homotypic cell to cell
adhesion on normal cells.55,56 EpCAM is a significant tumor antigen because its
overexpression has been observed in a majority of carcinomas including ovarian cancer,
breast cancer, prostate cancer, and nonsmall cell lung cancer.56 The inhibition of this antigen
has been associated with a decrease in the proliferation, migration, and invasion of cancer
cells, therefore making it an important target for cancer immunotherapy.
Go to:
Trifunctional antibodies
Trifunctional antibodies have a much higher capacity for tumor kill than previous monoclonal
antibody lines.57 Preclinical models have shown that the improved effectiveness of these
antibodies lies in the ability of the fragment crystallizable (Fc) and fragment antigen-binding
(Fab) portions of the antibody to trigger an immune response by interacting with EpCAM and
the cluster of differentiation (CD) 3. The trifunctional molecule can induce and recruit T
cells, as well as Fcγ-receptor+ accessory cells. Accessory cells are activated by an interaction
between the Fc region of the intact antibody and Fcγ receptors.58 This activation of
accessory cells leads to the secretion of cytokines such as IL-12, TNF-α, and the DC-specific
cytokine DC-CK1, as well as to the presentation of costimulatory molecules to the T cell.57
The formation of this complex induces the activation of different classes of effector T cells,
resulting in excellent antitumor activity. Another result of this process of immune activation
is that tumor material is phagocytosed,58 processed, and presented by professional antigen-
presenting cells.
Catumaxomab is one such trifunctional antibody. Clinically the efficacy of these trifunctional
molecules to generate antitumor immunity was shown in patients with gastric carcinoma (N =
9), administered infusions of either catumaxomab or ertumaxomab. Four weeks later the
patients were given irradiated tumor cells and were able to mount a significant T cell
response to these cells in five of nine patients.59

29
Catumaxomab: clinical trials
Malignant pleural effusions
Catumaxomab was evaluated in a phase I/II trial in patients with malignant pleural effusion
(MPE).55 Patients were given a series of three escalating doses of 5–200 μg catumaxomab
administered intrapleurally. Patients had effusions with cells positive for containing epithelial
cell adhesion molecule-positive cells. Twenty-four (11 breast, six lung [non-small cell lung
carcinoma (NSCLC)], three stomach, one ovarian, one carcinoma of unknown primary, one
esophageal) patients were treated with catumaxomab. Seven out of 24 patients (29%) treated
with catumaxomab reached the end of trial. Attrition was due to death from advanced
malignancy. Five of these seven patients showed a response to treatment according to the
criteria. This included one complete response and four partial responses. A complete response
was defined as relief of symptoms related to the effusion with absence of fluid
reaccumulation on chest radiographs. Partial response was defined as diminution of dyspnea
related to the effusion, with partial reaccumulation of fluid (<50% of the initial radiographic
evidence of fluid), with no further therapeutic thoracenteses required. Two patients had a
treatment failure and these were patients with NSCLC. All responses to treatment were
observed in patients with breast cancer. Most frequent adverse events were pyrexia, elevated
liver enzymes, nausea, and decreased lymphocytes. Dose-limiting toxicities were observed in
two patients: one had pleural empyema and fatal sepsis, and one had grade three erythema
and hepatobiliary disorder. Table 1 summarizes the therapy related adverse effects.

Table 1
Adverse effects of catumaxomab: pleural effusion trial
Malignant ascites
Catumaxomab was evaluated as part of a phase I/II dose-escalating study for intraperitoneal
application in patients with ovarian cancer who had EpCAM-positive tumor cells.60 Twenty-
three women with recurrent ascites due to pretreated refractory ovarian cancer were treated
with 4–5 intraperitoneal infusions of catumaxomab in doses of 10 to 200 micrograms within
9–13 days with loading doses of 5–10 μg. The maximum tolerated dose was defined at 10,
20, 50, 200, and 200 μg for the first through fifth doses. In dose group IIa, one patient had a
grade three serum bilirubin increase after the application of 50 μg. Therefore, the DSB
decided to reduce this second dose to 20 μg, and the protocol was amended accordingly. Side
effects included transient fever (83%), nausea (61%), and vomiting (57%), which were
considered either grade one or two in severity. A total of 39 grade three, and two grade 4,
treatment-related adverse events (AE), nine of them after the highest dose level (200 μg),
were observed in 16 patients. Most adverse effects were reversible without sequelae. Table 2

30
summarizes the AEs. Treatment with catumaxomab resulted in significant and sustained
reduction of ascites flow rate. A total of 22 of 23 patients did not require paracentesis
between the last infusion and the end of study one month later. Tumor cell monitoring
revealed a reduction of EpCAM-positive malignant cells in ascites by up to five log.

Table 2
Malignant ascites trial: grade three or greater toxicities
Adverse effects of catumaxomab
The adverse effects of catumaxomab have been found to be mainly secondary to cytokine
release. These include nausea, vomiting, abdominal pain, pyrexia, and skin reactions.4
Laboratory abnormalities have included elevated liver enzymes and lymphocytopenia. In the
phase I/II intraperitoneal trial by Burges and co-workers,60 fever (83%) was the predominant
AE; other AEs included nausea (61%), vomiting (57%), -and abdominal pain (37%). Most of
these adverse effects occurred on the day of or the day after infusion and were fully
reversible.60 Liver function abnormalities of gamma-glutamyl transpeptidase (GGT) and
aspartate aminotransferase (AST) occurred 13% and 9% respectively. Hematologic toxicity
was characterized by lymphocytopenia in 26%. No data on anemia was available. Grade three
toxicities included fever, and liver function abnormalities. Two grade four toxicities included
GGT increase and one case of hyperuricemia. In the pleural effusion study55 where the drug
was given intrapleurally, the most common toxicities were pyrexia and hepatobiliary
disorders. Fever was no greater than grade two and was observed in 15 out of 24 patients,
with six patients each having fever in dose levels II (10–50 μg) and III (20–100 μg).
Hepatobiliary disorders were observed in the majority of patients and most (13 of 14 events)
were considered catumaxomab related. The mean values of GGT, alanine aminotransferase
(ALT), AST, and bilirubin showed a transient increase 24 hours after the first and second
infusion. The increase in the majority of cases did not exceed grade two and was highest after
the second infusion. There was no dose response relationship. Grade three and four elevations
of GGT occurred in nine (60%) and three (50%) patients in dose levels II and III,
respectively. No grade four elevation of AST or ALT was observed. In one and three patients
at dose levels II and III, respectively, grade three elevations of AST occurred. Two patients
developed grades three and four elevation of GGT in the follow-up period 8 days after the
third infusion; in one of the cases, a relationship to the study drug could not be ruled out by
the investigator. Both patients had systemic progression of disease as possible explanation for
the GGT elevation. Hematologic toxicity was primarily anemia and lymphopenia. Seven of
15 patients in dose level II (10–50 μg) and two of six patients in dose level III (20–100 μg)
had grade two anemia.55
Administration of catumaxomab

31
Experience with catumaxomab given systemically suggests that premedication with 1000 mg
paracetamol (orally or suppository) and use of an H1 and H2 blocker be used to minimize
febrile reactions and minimize risk for anaphylaxis.55,60 In the pleural effusion study 100
mL 0.9% NaCl solution was also infused into the pleural space via the infusion lumen of the
trocar catheter to help disperse antibody. In the malignant ascites study60 1,000 mg
paracetamol was given 30 minutes before the start of infusion. To improve the catumaxomab
distribution within the peritoneal cavity, 500 mL of 0.9% NaCl solution was administered
intraperitoneally 30 minutes before the start of the catumaxomab infusion to disperse the
antibody.
Conclusion
The use of trifunctional antibodies represents a new approach to the management of two
important complications associated with advanced cancer, namely, malignant pleural
effusions and malignant ascites. The effectiveness of catumaxomab in terms of markers of
palliation such as decreased need for paracentesis and thoracentesis is evident even in the
early studies with this tri-functional antibody. The toxicities experienced by the patients in
these studies, while partly attributable to the antibody itself, may also be evidence of the
rapid tumor progression in this patient population. The harnessing of the immune system
suggests that this antibody may not only be effective for advanced disease but may also be
beneficial for patients with earlier stages of disease. The analogy would be the use of
rituximab in conjunction with chemotherapy to improve survival in patients with lymphoma.
Further work in a broad spectrum of EpCam-positive tumors may very well bear witness to
the effectiveness of this unique molecular therapy.

32
REFERENCE B

Cirrhosis of the liver is a chronic disease that causes cell destruction and fibrosis (scarring)
of hepatic tissue. Fibrosis alters normal liver structure and vasculature, impairing blood and
lymph flow and resulting in hepatic insufficiency and hypertension in the portal vein.
Complications include hyponatremia, water retention, bleeding esophageal varices.
Coagulopathy, spontaneous bacterial peritonitis, and hepatic encephalopathy.

Cirrhosis is a potentially life-threatening condition that occurs when scarring damages the
liver. This scarring replaces healthy tissue and prevents the liver from working normally.
Cirrhosis usually develops after years of liver inflammation. When chronic diseases cause the
liver to become permanently injured and scarred, the condition is called Cirrhosis. Cirrhosis
harms the structure of the liver and blocks the flow of blood. The loss of normal liver tissue
slows the processing of nutrients, hormones, drugs, and toxins by the liver. Also, the
production of proteins and other substances made by the liver is suppressed. People with
cirrhosis often have few symptoms at first. The person may experience fatigue, weakness,
and exhaustion. Loss of appetite is usual, often with nausea and weight loss. As liver function
declines, water may accumulate in the legs and the abdomen (ascites). A decrease in proteins
needed for blood clotting makes it easy for the person to bruise, bleeding or infection. In the
later stages of cirrhosis, jaundice (yellow skin) may occur, caused by the buildup of bile
pigment that is passed by the liver into the intestines. The liver of a person with cirrhosis also
has trouble removing toxins, which may build up in the blood. Drugs taken usually are
filtered out by the liver, and this cleansing process also is slowed down by cirrhosis. People
with cirrhosis often are very sensitive to medications and their side effects. The doctor often
can diagnose cirrhosis from the patient’s symptoms and from laboratory tests. During a
physical exam, the doctor could notice a change in how your liver feels or how large it is. If
the doctor suspects Cirrhosis, you will be given blood tests. The purpose of these tests is to
find out if liver disease is present. In some cases, other tests that take pictures of the liver are
performed such as the computerized axial tomography (CAT) scan, and ultrasound. The
doctor may decide to confirm the diagnosis by putting a needle through the skin (biopsy) to
take a sample of tissue from the liver. In some cases, cirrhosis is diagnosed during surgery
when the doctor is able to see the entire liver.

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ANATOMY AND PHYSIOLOGY:

The liver is located in the upper right-hand portion of the abdominal cavity, beneath the
diaphragm and on top of the stomach, right kidney and intestines. The liver, a dark reddish-
brown organ that weighs about 3 pounds, has multiple functions.

There are two distinct sources

that supply blood to the liver:
• oxygenated blood flows
in from the hepatic artery
• nutrient-rich blood flows
in from the portal vein
•
The liver holds about one pint (13
percent) of the body’s blood
supply at any given moment.

The liver consists of two main

lobes, both of which are made up of thousands of lobules. These lobules are connected to
small ducts that connect with larger ducts to ultimately form the hepatic duct. The hepatic
duct transports the bile produced by the liver cells to the gallbladder and duodenum (the first
part of the small intestine).
The liver regulates most chemical levels in the blood and excretes a product called “bile,”
which helps carry away waste products from the liver. All the blood leaving the stomach and
intestines passes through the liver. The liver processes this blood and breaks down the

34
nutrients and drugs into forms that are easier to use for the rest of the body. More than 500
vital functions have been identified with the liver. Some of the more well-known functions
include the following:

▪ Production of bile, which helps carry away waste and break down fats in the small
intestine during digestion.
▪ Production of certain proteins for blood plasma.
▪ Production of cholesterol and special proteins to help carry fats through the body.
▪ Conversion of excess glucose into glycogen for storage. (This glycogen can later be
converted back to glucose for energy.)
▪ Regulation of blood levels of amino acids, which form the building blocks of proteins.
▪ Processing of hemoglobin for use of its iron content. (The liver stores iron.)
▪ Conversion of poisonous ammonia to urea. (Urea is one of the end products of protein
metabolism that is excreted in the urine.)
▪ Clearing the blood of drugs and other poisonous substances.
▪ Regulating blood clotting.
▪ Resisting infections by producing immune factors and removing bacteria from the
blood stream.

When the liver has broken down harmful substances, its by-products are excreted into the bile
or blood. Bile by-products enter the intestine and ultimately leave the body in the feces.
Blood by-products are filtered out by the kidneys, and leave the body in the form of urine.

PREDISPOSING FACTORS:
1. Chronic Alcoholism
2. Malnutrition – decrease Vitamin B, thiamin – main cause
3. Virus
4. Toxicity – e.g. carbon tetrachloride
5. Use of hepatotoxic agents

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SIGNS AND SYMPTOMS:

I. Early Signs
• Weakness, fatigue
• Anorexia
• Stomatitis
• Urine – tea color
• Stool – clay color
• Hepatomegaly
• Jaundice
• Pruritus or urticaria

II. Late Signs

A. Hematological changes – all blood cells decrease
• Leukopenia – decrease
• Thrombocytopenia – decrease
• Anemia – decrease
B. Endocrine changes
• Spider angiomas, Gynecomastia
• Caput medusa, Palmar errythema
C. GIT changes
• Ascitis, bleeding esophageal varices – due to portal Hypertension
D. Neurological Changes

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PATHOPHYSIOLOGY:

Cirrhosis is characterized by diffuse fibrotic bands of connective tissue that distort the liver’s
normal architecture. Inflammation caused by either toxins or disease results in extensive
degeneration and destruction of hepatocytes ( liver cells ). As cirrhosis develops, the tissue
becomes nodular. These nodules can block lile ducts and normal blood flow throughout the
liver. Flow alterations in the vascular system and lymphatic bile duct channels result from
compression caused by the proliferation of fibrous tissue. In early disease, the liver is usually
enlarged, firm and hard. As the pathologic process continues, the liver shrinks in size.

COMPLICATIONS:
Cirrhosis is the eleventh leading cause of death by disease in the United States, killing more
than 25,000 people each year. A damaged liver affects almost every bodily process, including
the functions of the digestive, hormonal, and circulatory systems. The most serious
complications are those associated with so-called decompensation, which occur when
cirrhosis progresses. They include the following:
▪ Bleeding and fluid buildup (ascites).

37
 ▪ Infections.
▪ Damage to the brain (encephalopathy). Impaired brain function occurs when the liver
cannot detoxify harmful substances.

Liver cancer is also a long-term risk with cirrhosis.

Cirrhosis is irreversible, but the rate of progression can be very slow, depending on its cause
and other factors. Five-year survival rates are about 85% and can be lower or higher
depending on severity.

▪ For example, alcoholics with cirrhosis who abstain can have a 5-year or more survival
rate of as high as 85%. For those who continue drinking, the chance for living beyond
5 years is no higher than 60%.
▪ In patients with hepatitis B or C, the 5-year survival rate after a diagnosis of cirrhosis
ranges between 71 – 85%.
▪ About two-thirds of patients with primary biliary cirrhosis never develop symptoms
and can have a normal life span. Once symptoms of liver damage, such as jaundice,
occur, however, the average survival time declines. In one study of women diagnosed
with primary biliary cirrhosis, about 36% developed symptoms over an 11-year
period, and 11% either died or required liver transplantation.

1. Portal Hypertension
In cirrhosis, liver cell damage slows down blood flow. This causes a backup of blood through
the portal vein, a condition called portal hypertension . The effects of portal hypertension can
be widespread and serious, including fluid buildup and bleeding.

2. Ascites and Fluid Buildup. Ascites is fluid buildup in the abdomen. It is uncomfortable
and can reduce breathing function and urination. Ascites is usually caused by portal
hypertension, but it can result from other conditions. Swelling can also occur in the arms and
legs and in the spleen. Although ascites itself is not fatal, it is a marker for severe
progression. Once ascites occurs, only half of patients survive after 2 years. In fact, some
experts refer to the phases of cirrhosis aspreascitic and ascitic . Some doctors even believe
that ascites signals the need for liver transplantation, particularly in alcoholic cirrhosis.

3. Variceal Bleeding. One of the most serious repercussions of portal hypertension is the
development of varices , which are blood vessels that enlarge to provide an alternative
pathway for blood diverted from the liver. In about two-thirds of patients they form in
esophagus. Varices pose a high risk for rupture and bleeding because of the following
characteristics:

38
 ▪ They are thin-walled.
▪ They are often twisted.
▪ They are subject to high pressure.
▪ Internal bleeding from these varices (variceal bleeding) occurs in 20 – 30% of patients
withcirrhosis. The risk of death from a single episode can reach 70%.

Bleeding commonly recurs within 2 weeks of the first episode, but after 6 weeks, the risk for
recurrence is the same as for patients who have not had a bleeding event.

Factors that predict variceal bleeding include:

▪ Ascites.
▪ Encephalopathy.
▪ Large veins.

Factors that can increase the danger for a bleeding episode in high-risk individuals include
the following:
▪ Moderate to intense exercise.
▪ Bacterial infection.
▪ Certain times of the day. Eating increases portal pressure, and there is a greater risk
for bleeding in the evening. A lesser but still significant risk occurs in the early
morning.

It is important for patients to be screened for esophageal varices and treated with preventive
beta blockers if they show signs of risk. Between 30 – 40% of patients
with cirrhosis experience bleeding. this complication has a mortality rate of 20 – 35%. Some
experts recommend that all newly diagnosed patients be screened using endoscopy. Screening
should also be considered for all previously diagnosed patients who have not been screened
but would benefit from preventive treatments.

4. Kidney Failure
Portal hypertension can cause several secondary complications, including kidney failure.
Non-steroidal anti-inflammatory drugs (NSAIDs), such as naproxen, may increase the risk
for kidney failure.

5. Gastrointestinal Bleeding

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Gastrointestinal (GI) bleeding can occur from abnormal blood clotting, which can be result of
a combination of complications associated with cirrhosis. They include vitamin K
deficiencies and thrombocytopenia — a drop in platelets (the blood cells that normally
initiate the clotting process). Some research now suggests that thrombocytopenia itself may
be associated with more advanced liver failure.

6. Infections
Bacterial infections are very common in advanced cirrhosis, and may even increase the risk
for bleeding. Most bacterial infections, including those in the urinary, respiratory, or
gastrointestinal tracts, develop when patients are in the hospital. Abdominal infections are a
particular problem incirrhosis and occur in up to 25% of patients with cirrhosis within a year
of diagnosis.

7. Mental Impairment and Encephalopathy

Mental impairment is a common event in advanced cirrhosis. In severe cases, the disease
causes encephalopathy (damage to the brain), with mental symptoms that range from
confusion to coma and death. A combination of conditions associated with cirrhosis causes
this serious complication:
▪ Buildup in the blood of harmful intestinal toxins, particularly ammonia.
▪ An imbalance of amino acids that affect the central nervous system.

Encephalopathy is often triggered by certain conditions, including:

▪ Gastrointestinal bleeding
▪ Constipation
▪ Excessive dietary protein
▪ Infection
▪ Surgery
▪ Dehydration

Alcoholics with cirrhosis are believed to be at higher risk for this complication than are
nonalcoholic cirrhosis, but one study suggested that alcoholics simply tend to have more
severecirrhosis. Even minimal hepatic encephalopathy (MHE) can have detrimental effects
on functional ability. One study suggested that MHE impairs the ability to safely drive a car,
and that all patients with cirrhosis be tested for MHE.

40
DIAGNOSTIC EVALUATION:

▪ Liver biopsy – detects destruction and fibrosis of hepatic tissue.

▪ Liver scan – shows abdominal thickening and a liver mass.
▪ CT scan – determines the size of the liver and its irregular nodular surface.
▪ Esophagoscopy – to determine esophageal varices.
▪ Paracentesis – to examine ascetic fluid for cell, protein, and bacterial counts.
▪ PTC – differentiates extrahepatic from intrahepatic obstructive jaundice.
▪ Laparoscopy and liver biopsy – permit direct visualization of the liver.
▪ Serum liver function test – results are elevated

NURSING INTERVENTIONS:

Promoting Activity Tolerance

▪ Encourage alternating periods of rest and ambulation.
▪ Maintain some periods of bed rest with legs elevated to mobilize edema and ascites.
▪ Encourage and assist with gradually increasing periods of exercise.

Improving Nutritional Status

▪ Encourage patient to eat high calorie, moderate protein meal and to have
supplementary feedings.
▪ Suggest small, frequent feedings and attractive meals in an aesthetically pleasing
setting at meal time.
▪ Encourage and assist withgradually increasing periods of exercise.

Protecting Skin Integrity

▪ Note and record degree of jaundice of skin and sclerae and scratches on the body.
▪ Encourage frequent skin care, bathing without soap, and massage with emollient
lotions.
▪ Advise patient to keep fingernails short.

41
Patient Education and Health Maintenance
▪ Stress the necessity of giving up alcohol completely.
▪ Urge acceptance of assistance from a substance abuse program.
▪ Provide written dietary instructions.
▪ Encourage daily weighing for self-monitoring of fluid retention depletion.
▪ Discuss adverse effects of diuretic therapy.
▪ Emphasize the importance of rest, a sensible lifestyle, and an adequate, well-
balanced diet.
▪ Involve the person closest to the patient because recovery usually is not easy and
relapses are common.
▪ Stress the importance of continued follow –up for laboratory test and evaluation by a
health care provider

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DISCUSSION
SIMLARITIES
Real case, Reference A and Reference B
Based on my case study, there have a few similarity I found in real case, Reference A and B.
First similarity want to discuss is the sign and symptoms ascites. These three cases said fluid
overload started with having shortness of breath which caused by fluid in the lungs, cough,
swelling in the legs or arms, abdominal distension or swelling, changes in the blood pressure
which caused by excess fluid in the bloodstream and increased or slow heart rate.
Next similarity from these cases is the investigation of ascites. Real case, reference A and B
used patient’s history for their investigation. The doctor will ask about patient’s personal and
family medical history as well as recent and current symptoms which may help them to relate
recent diagnosis with the medical history. Next same investigation used by these three cases
is the physical exam. The physical examination is the process by which a medical
professional investigates the body of a patient for signs of disease. It generally follows the
taking of the medical history which an account of the symptoms as experienced by the
patient. During physical examination, doctor will inspect whether the patient is alert,
conscious, pale or pink and have good or poor hydration. Not only that, doctor also palpate
all upper and lower limb to see whether have any abnormality and carry out the percussion
where doctor will tapping body parts with fingers, hands to determine the size and boarders
of body organs . Next doctor will auscultate the lungs to listen the sounds in lungs. For
example, when auscultate patient with fluid overload, we can hear crepitation sound at base
of the lungs.
Not only that, according to the laboratory test, these three cases used full blood count (FBC).
Full blood count is one of the test used to evaluate overall health and detect a wide range of
disorders, including anaemia, infection and leukaemia. This test also help to measures several
components and features of blood. Next laboratory test used by this cases is liver function test
(LFT). Liver function tests are groups of blood tests that give information about the state of a
patient's liver. These tests include protein levels, prothrombin time, aPTT, albumin, bilirubin,
and others.
Other same investigation used by real case and the references is renal profile test (RP) and
arterial blood gases (ABG) which is a blood test that measures the acidity, or pH, and the
levels of oxygen (O2) and carbon dioxide (CO2) from an artery. The test is used to check the
function of the patient's lungs and how well they are able to move oxygen and remove carbon
dioxide.
Other same investigation used by real case and the references is an electrocardiogram (ECG)
which help for heart’s electrical activity and will identify the heart rate and rhythm, and
display existing arrhythmias, hypertrophy, and ischemia. and chest x-ray which used by
doctor to view the inside of body without having to make an incision and this also help them
to diagnose, monitor and treat many medical conditions. Not only that, chest x-ray also will
depict oedema and underlying disease such a pneumonia.

43
Next similarity I found from these three cases is the treatment and management of fluid
intake. Reducing the intake of fluids especially to congestive heart failure one of the
treatment used in these cases. In the hospital, the doctor may order less IV fluids or restrict
fluid intake. At home, the doctor may only let patient have up to 2 litres a day of fluids or less
depending on the amount of swelling. Reduced- salt intake also other similar treatment used
in this three cases. For example if the patient have heart, kidney or liver conditions, they may
need to follow a reduced-salt diet. This helps keep sodium levels within normal limits, which
helps avoid from hypervolemia.
In conclusion, we can understand that the real case, reference A and B are used same sign and
symptoms, medical history, physical examination, full blood count, liver function test (LFT),
renal profile, arterial blood gases , electrocardiogram and chest x-ray exam, reduced fluid
and salt intake for fluid overload.

DIFFERENCES
Real case, Reference A and Reference B
Based on my case study, there also have a few differences found in real case, reference A and
B. First difference I found from these cases is the investigation of fluid overload. For
example, according to laboratory radiology test, real case used urine FEME which is a test of
urine. A urinalysis is used to detect and manage a wide range of disorders, such as urinary
tract infections, kidney disease and diabetes. A urinalysis involves checking the appearance,
concentration and content of urine. Abnormal urinalysis results may point to a disease or
illness.
Next, different test used in real case is glucose test (DXT). Many types of glucose tests exist
and they can be used to estimate blood sugar levels at a given time or, over a longer period of
time, to obtain average levels or to see how fast body is able to normalize changed glucose

44
levels. Eating food for example leads to elevated blood sugar levels. This tests are not
mentioned in both references.
But other different investigation used by authors in both references is the echocardiography.
Echocardiography uses standard two-dimensional, three-dimensional, and Doppler ultrasound
to create images of the heart and this also one of the most important investigation. This is
because, it will provide critical information about the heart performance, the wall
measurement and the presence of heart disease. Beside echocardiography, B-type natriuretic
peptide (BNP) test also used to diagnose cardiac failure. This investigations are not
mentioned in real case.
Next difference found from real case and the references is the treatment of ascites. Both
reference A and B are used water-pill or diuretics for treat hypervolemia which may help the
body to pull off excess fluid. Diuretics can deplete potassium and it may need to be replaced.
For instance, someone with heart failure may need to take steps to manage their condition in
addition to taking diuretics. But some said diuretics may not work for people with severe
kidney problems and they need dialysis. This treatment is not mentioned in real case.
Next different treatment and management used in reference A is keeping swollen feet
elevated above the level of heart. This will prevent pooling of fluids in the lower legs, ankles
and feet. Patient have to wear compression stockings until the swelling is control. But when
the patient is in sitting position, ask them to make their feet up, and try some ankle exercise to
increase the blood circulation. Beside this, author in reference A also suggest patient who has
fluid overload, to eat asparagus or drink asparagus water. Asparagus is a natural diuretic and
can help the body release excess fluid naturally. This treatment and management is not used
in reference B and real case.
While according to pharmacology treatment, doctors in real case prescribed medications like
IV Ranitidine 50mg stat, IV Lasix 40mg Stat/ IV Frusemide 40mg TDS, Human Albumin
200g/ml.
In conclusion, we can understand that these three cases are used different investigations like
urine FEME, glucose test, B-type natriuretic peptide (BNP), echocardiography, treatments
and pharmacology drugs.

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CONCLUSION
As a conclusion we get know that fluid abdominal accumulation also known as ascites, is a
condition in which there is an excess of fluid volume in the intravascular compartment. It is
either caused by increased fluid intake, diseases that lead to sodium and water retention, or
phenomena that promote the influx of fluid into the plasma. For example, congestive heart
failure (CHF), renal failure, and liver failure may lead to impairment of sodium handling.
Furthermore, treatment with albumin or hypertonic solutions results in the intravascular shift
of fluids.
The clinical picture and physical examination will reflect the abnormal fluid status.
Furthermore, the patients will likely exhibit signs and symptoms of pulmonary oedema and
CHF in addition to features of underlying pathologies.
The clinician should obtain a detailed history and perform a full evaluation of the patient's
presentation and physical assessment. Moreover, key laboratory tests and imaging techniques
are pertinent components of the workup. The later will help identify the etiology of the
ascites. Prompt diagnosis and treatment are paramount for the prevention of overload
progression.
Treatment involves fluid restriction, possible use of diuretic therapy, and dietary
modifications. Furthermore, iatrogenic causes such as excessive fluid resuscitation may be
avoided with careful treatment especially in the elderly and those with cardiac and renal
dysfunction.
While according to World Health Organization, profound acute kidney injury (AKI) is
complicated by fluid overload, which was initially demonstrated in children who underwent
bone marrow transplantation. In fact, 70% of patients of the study warranted dialysis as they
did not exhibit renal improvement. Similarly, hypervolemia was prevalent in paediatric
populations who needed continuous renal replacement therapy.
According to these studies, the severity of overload in itself is indicative of poor outcomes
and fatality. The survivors' treatment course was associated with a delay in renal recovery
and a prolonged duration of hospitalization and mechanical ventilation
Collectively, these investigations concluded that the presence of ascites is significant
in kidney failure. Hence, the excessive fluid volume should be corrected to prevent morbidity
and mortality.
Not only that, beside learned about fluid overload, during posting in Emergency department, I
got chance to observe the fluid removal procedure that was done by the doctor. I gained
knowledge in depth by comparing the care with patient, I collected information from internet,
doctors, ward sisters, nurses, lab, radiology and record section and compared it with patient in
real situation. During my duty period in emergency department, I provided her a holistic care,
diversional therapy in very aspects like physical, emotional, economical and socio-cultural
view.
I also gained the knowledge about the Medical Assistant theory and application in real
situation. So, this case, not only gives the cognitive domain but also provides us the
opportunity to develop psychomotor domain, which is very important in Medical Assistant
course, so the patient is the main source of conveying knowledge in practical.

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Reference:-
• https://emedicine.medscape.com/article/80944-overview
• https://www.cochranelibrary.com/es/cdsr/doi/10.1002/14651858.CD013123/full/es
• https://gi.org/topics/ascites/
• https://www.sciencedirect.com/science/article/pii/S1726490112003127
• https://www.msdmanuals.com/professional/SearchResults?query=hypervolemia
• https://www.healthresource4u.com/hypervolemia.html
• https://patient.info/doctor/fluid-overload

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