Case Write Up Acute Pancreatitis

Rasyidah binti Rustam | 57260211004
Year 3 MBBS UniKL/VMU | 2011/2016
UNIVERSITI KUALA LUMPUR (UNIKL)

ROYAL COLLEGE OF MEDICINE PERAK (RCMP)
SURGERY POSTING
CASE WRITE-UP
Name : Rasyidah binti Rustam

Matric No. : 57260211004
Group : Group 3 MBBS Year 3 2011/2016
Supervisor : Assoc. Prof. Dr. Tin Win
1
Identification data:
Name : Mr. S
Age : 15
Sex : Male
Race : Malay
Address : Pasir Puteh, Ipoh
Marital status : Single
Occupation : Student
Hospital registration no. : HRPB 5200516
NRC no. : 980618-08-6325
Date of admission : 12th December 2013
Date of clerking : 15th December 2013
Date of discharge : 16th December 2013
Chief complaint
Abdominal pain three days prior to admission.
History of presenting illness
Patient was apparently well until August 2013, when he was admitted to the hospital due to
abdominal pain and he was diagnosed to have acute pancreatitis. Three days prior to
admission, he presented with the same complaint of abdominal pain. The site of the pain was
at the epigastric region. It was sudden onset and the pain became worse on the day of
admission, 12th December 2013. It was throbbing pain in nature and it radiated to his back. It
was associated with low grade fever and no chill and rigor. Other than that, he had nausea and
vomiting. He had 5 episodes of vomiting. It was a non-projectile vomiting. The vomitus was
contained food particles, no blood stained and no bile pigments. It was about one small bowl
in quantity per vomiting. The pain occured continously the entire day and get worsen at night.
The pain was aggravated by eating, drinking and lying flat. It was relived by bending foward.
The severity of the pain is 6/10.
2
Mr. S was brought by his sister to the casuality due to his abdominal pain. In the casuality, he
was put at the proper area. He was given painkiller. X-ray was done. Blood sample was taken
for laboratory investigation. Vital signs were taken. After that, admission to ward 2A/08.
Systemic Review
Respiratory system No difficulty in breathing, no cough, no

asthma.
Central nervous system No headache, no giddiness, no vertigo
and no loss of consciousness.
Cardiovascular system No chest pain, palpitation
Gastrointestinal system Loss of appetite, no weight loss, no
diarrhea, no constipation, no change in
bowel habits and no dysphagia.
Genitourinary system No change in frequency of urination, no
polyuria, no oliguria, no hematuria, no
pain during micturition, no incontinence.
Musculoskeletal system No muscle weakness, no current joint
pain, no swellings.
Skin No skin rashes, no excessive sweating, no
night sweat.
Table 1 : Systemic review of Mr. S
Past medical history
Patient is a known case of hyperlipidemia since September 2013. He is not under follow-up.
No history of diabetes mellitus, hypertension and heart diseases.
Past surgical history
No known past surgical history. No history of past invasive procedure eg. ERCP
Drug history
Patient is on T. Lovastatin 20mg. He is not compliance to the drugs.
3
Allergy history
There is no known drugs, food and environment allergy.
Family history
Mr. Ss father is 52 years old, working as businessman and a known case of hyperlipidemia.
His father has no history of asthma, diabetes mellitus, hypertension and ischemic heart
disease.
Mr. Ss mother is 48 years old. She is a housewife. His mother has no comorbids.
Mr. S is the 6th child out of 7 siblings. All his siblings are healthy and fits.
Social history
Mr. S is a non-smoker and non-alcholic. Currently living with his parents and siblings at Pasir
Puteh with good electricity, water and sewage sources. Recently does not travel to any places.
No history of intravenous drugs used.
4
Physical examination
General Examination
The patient is lying flat comfortably in supine position. He does not look ill. He is concious
and alert to time, place and person. He is not in respiratory distress and his hydrational and
nutritional status is adequate. No muscle wasting and no abnormal movements. There is a
cannula attached to the dorsum of his left hand and a urine bag is attached at the right side of
the bed. He is overweight.
Vital signs
Temperature : 37C
Pulse : 64 beats per minute, regular rhythm and good volume
Respiratory rate : 20 breaths per minute
Blood pressure : 130/80 mmHg
Hands
The patients palms were pink. There were no finger clubbing, no palmar erythema,no
leukonycia, no koilonycia and no muscle wasting. The capillary refill time < 2 secs.
Face
No jaundice, conjuntiva is pale. The patients oral hygiene was fair. No brownish
discolouration of the tongue. There were no angular stomatitis or glossitis.
Neck
There were no lymph nodes enlargement, no swelling, no thyroid enlargement and no

increased in jugular venous pressure
Feet
There was no pitting edema.
5
1. Abdominal Examination
Inspection
There was no abdominal distension, no dilated vein, no scars, and no striae, no discolouration
of skin. The umbilicus was inverted and centrally located and his abdomen move with
respiration. There was no visible cough impulse.
Palpation
Superficial : The abdomen was rigid with tenderness at the epigastric region. There was
guarding, no rebound tenderness.
Deep : There was tenderness at the epigastric region. There were no palpable masses or
organs.
Liver : The liver was not palpable.
Spleen : The spleen was not palpable.
Kidneys : Both the left and right kidneys were not ballotable.
Percussion
Liver : The patients liver span was 12.5 cm, which is mild hepatomegaly.
Spleen : Traubes space was resonant, no splenomegaly.
There was no shifting dullness and no fluid thrill.
Auscultation
Bowel sounds were heard 3 times per minute which was normal. There were no kidney bruits.
Per rectal examination
The prostate was smooth and firm, the median sulcus was prominent and there were no lobe
enlargements. There were no masses, swellings or ulcers on the rectal wall.
6
2. Cardiovascular Examination
First and second heart sound are heard with normal intensity. There are no mummurs heard.
3. Respiratory Examination
Vesicular breath sound in both lungs was heard. The lungs were clear, no stridor, wheezing
and crackles heard.
Summary
A 15-year-old Malay boy with known case of acute pancreatitis and hyperlipidemia, presented
with abdominal pain three days prior to admission and associated with fever, nausea and
vomiting.
Provisional diagnosis
Acute pancreatitis.
This is because the patient presented with sudden onset of epigastric pain that radiated to the
back which is throbbing pain in nature and exaggerated by eating and drinking but relieved by
bending foward. The duration of pain is more than a day. It is associated with nausea and
vomiting and as well as fever.
Differential diagnosis
Acute mesentric ischemia
Reason: Patient complained of upper abdomen pain that usually diffuse, constant or
sometimes colicky. It is associated with nausea, vomiting, abdominal distention, diarrhea and
fever.
Cholecystitis
Reason: Patient presented with upper abdominal pain that radiated to the right shoulder or
scapula. Nausea and vomiting are generally present and patients may have fever.
Cholangitis
Reason: Patient presented with fever, right upper quadrant pain and jaundice
7
Chronic pancreatitis
Reason: Patient presented with early onset of abdominal pain and it often in the midabdomen
and occasionally radiating in a bandlike fashion or localized to the back. The pain occur either
after meals or independently of meals. It can presented with diarrhea and weight loss.
Pancreatic cancer
Reason: Patient presented with gradual onset of symptoms such as anorexia, malaise, nausea,
fatigue and midepigastric or back pain that radiated to the back. It is often night time pain and
may increased discomfort after eating. The pain may be worse when the patient is lying flat.
8
Investigation
Full blood count (FBC)
Patients value Normal value Interpretation

3
WBC (10 / microL) 17.3H 0.0 -11.0 High
HGB (g/dL) 14.8 13.0-18.0 Normal
HCT (%) 43.6 40.0 52.00 Normal
MCV (fL) 72.9L 76.0 96.0 Low
MCH (pg) 24.7L 27.0 32.0 Low
MCHC (g/dL) 33.9 30.0 35.0 Normal
3
Platelets (10 / microL) 298 0 400 Normal
Neutrophils % 79.4H 40 75 High
9
Neutrophils (10 /L) 13.77H 0-7.0 High
Monocytes% 9.6H 2 10.0 Normal
Monocyte 1.66H 2-10 Low
Lymphocytes % 10.7 20 45.0 Low
9
Lymphocytes (10 /L) 1.85 0-3.0 Normal
Eosinophils % 0.2L 1-6 Low
9
Eosinophils (10 /L) 0.04 02-0.5 Normal
Basophils % 0.1 0-1 Normal
9
Basophils (10 /L) 0.02L 02-0.1 Normal
Favourable to be microcytic hypochromic anemia.
Amylase test
Patients Value Normal Value Interpretation

Amylase 1295 28-100 High
Favourable to be acute pancreatitis.
Urine diastase test

Diastase, urine 90 0-460 Normal
Glucose test

Glucose 6.6 <7.0 Normal
9
Liver Function Test (LFT)

Total protein 87 64-83 High
Total bilirubin 11.3 1-17 Normal
Alkaline phosphatase 101 1-390 Normal
Albumin 51 32-45 High
AST (SGOT) 15 0-40 Normal
Alanine Transaminase (ALT) 26 0-41 Normal
Globulin 36
Renal profile
NORMAL RANGE RESULT

Urea 1.7 8.3 3.0L (Normal)
Sodium 136 145 140 (Normal)
Potassium 3.5 4.5 4.2L (Normal)
Chloride 98 - 107 95 (Low)
Creatinine 50-77 69 (Normal)
Arterial Blood Gas (ABG)

Blood pH 7.367 7.35-7.45 Normal
CO2 pressure 38.40 L 35.0-45.0 Normal
O2 pressure 88.2 L 80.0-100.00 Normal
Bicarbonate actual, HCO3 21.6 L 21.0-25.0 Normal
Bicarbonate standard, HCO3 21.60
Base excess (ecf) Beecf -3.80 L -3.00-3.00 Low
Base excess (B), BE(B) -3.3
O2 saturation 96.3 L 95-98 Normal
Total CO2 (tCO2) 18.9 L 22.00-26.00 Low
Chest Xray (CXR)
Result: no free intraperitoneal air, lung field are clear, no cardiomegaly.
Abdomen Xray (AXR)
Result: no dilated bowels, no gallstones, Riglers sign is negative.
10
Final diagnosis
Recurrent acute pancreatitis.
Daily progress of the patient
12th December 2013
The patient was alert and conscious, and has intermittent pain at epigastric region. There is no
discolouration of skin noticed. There were no nausea and vomiting. The patient hydration is
fair, no pedal edema and per rectal examination was done, browish coloured stool noted.. On
palpation, the abdomen is rigid, no mass palpable and there was tenderness at epigastric
region.
Vital signs :
Temperature: 37.4C
Pulse: 103 beats per minute, regular rhythm and good volume
Respiratory rate: 20 breaths per minute
Blood pressure: 136/79 mmHg
13th December 2013
The patient was alert and conscious, not in respiratory distress and has generalised abdominal
pain especially at epigastric region. There is no discolouration of skin noticed. There were no
nausea and vomiting. The patient hydration is fair, no pedal edema and per rectal examination
was done, browish coloured stool noted. On palpation, the abdomen is rigid, guarding, no
mass palpable and there was tenderness at epigastric region.
Vital signs :
Temperature: 37C
11
14th December 2013
Vital signs :
Temperature: 37C
Pulse : 96 beats per minute, regular rhythm and good volume
15th December 2013
Vital signs :
Temperature: 37C
16th December 2013
The patient was alert and conscious, not in respiratory distress and has no generalised
abdominal pain. There is no discolouration of skin noticed. There were no nausea and
vomiting,. The patient hydration is fair, no pedal edema and per rectal examination was done,
browish coloured stool noted.. On palpation, the abdomen is soft, no guarding, no mass
palpable and non-tender.
12
Vital signs :
Temperature: 37C
13
Discussion
Pancreatitis is inflammation of the gland parenchyma of the pancreas. For clinical purposes, it
is useful to divide pancreatitis into acute, which presents as an emergency, and chronic, which
is prolonged and frequently lifelong disorder resulting from the development of fibrosis
within the pancreas.
Acute pancreatitis is defined as an acute condition presenting with abdominal pain and is
usually associated with raised pancreatic enzyme levels in the blood or urine as a result of
pancreatic inflammation. Acute pancreatitis may recur.
The underlying mechanism of injury in pancreatitis is thought to be premature activation of

pancreatic enzymes within the pancreas, leading to a process of autodigestion. Anything that
injures the acinar cell and impairs the secretion of zymogen granules, or damages the duct
epithelium and thus delays enzymatic secretion, can trigger acute pancreatitis. Once cellular
injury has been initiated, the inflammatory process can lead to pancreatic oedema,
haemorrhage and, eventually, necrosis.
As inflammatory mediators are released into the circulation, systemic complications can arise,
such as haemodynamic instability, bacteraemia (due to translocation of gut flora), acute
respiratory distress syndrome and pleural effusions, gastrointestinal haemorrhage, renal
failure and disseminated intravascular coagulation (DIC).
Acute pancreatitis may be categorised as mild or severe. Mild acute pancreatitis is

characterised by interstitial oedema of the gland and minimal organ dysfunction. Eighty per
cent of patients will have a mild attack of pancreatitis, the mortality from which is around 1%.
Severe acute pancreatitis is characterised by pancreatic necrosis, a severe systemic
inflammatory response and often multi-organ failure.
In those who have a severe attack of pancreatitis, the mortality varies from 20% to 50%.
About one-third of deaths occur in the early phase of the attack, from multiple organ failure,
while deaths occurring after the first week of onset are due to septic complications.
Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas

characterised by irreversible morphological change typically causing pain and/or permanent
loss of function. Many patients with chronic pancreatitis have exacerbations, but the condition
may be completely painless.
14
Possible causes of acute pancreatitis:
Gallstones
Alcoholism
Post ERCP
Abdominal trauma
Following biliary, upper gastrointestinal or cardiothoracic
Surgery
Ampullary tumour
Drugs (corticosteroids, azathioprine, asparaginase, valproic acid, thiazides,
oestrogens)
Hyperparathyroidism
Hypercalcaemia
Pancreas divisum
Autoimmune pancreatitis
Hereditary pancreatitis
Viral infections (mumps, coxsackie B)
Malnutrition
Scorpion bite
Idiopathic
Clinical Presentation
Pain is the cardinal symptom. It characteristically develops quickly, reaching maximum

intensity within minutes rather than hours and persists for hours or even days. The pain is
frequently severe, constant and refractory to the usual doses of analgesics. Pain is usually
experienced first in the epigastrium but may be localised to either upper quadrant or felt
diffusely throughout the abdomen.
There is radiation to the back in about 50% of patients, and some patients may gain relief by
sitting or leaning forwards. The suddenness of onset may simulate a perforated peptic ulcer,
while biliary colic or acute cholecystitis can be mimicked if the pain is maximal in the right
upper quadrant. Radiation to the chest can simulate myocardial infarction, pneumonia or
pleuritic pain. In fact, acute pancreatitis can mimic most causes of the acute abdomen and
should seldom be discounted in differential diagnosis.
Nausea, repeated vomiting and retching are usually marked accompaniments. The retching
may persist despite the stomach being kept empty by nasogastric aspiration. Hiccoughs can be
troublesome and may be due to gastric distension or irritation of the diaphragm.
On examination, the appearance may be that of a patient who is well or, at the other extreme,
one who is gravely ill with profound shock, toxicity and confusion. Tachypnoea is common,
tachycardia is usual, and hypotension may be present. The body temperature is often normal
or even subnormal, but frequently rises as inflammation develops. Mild icterus can be caused
by biliary obstruction in gallstone pancreatitis, and an acute swinging pyrexia suggests
15
cholangitis. Bleeding into the fascial planes can produce bluish discolouration of the flanks
(Grey Turners sign) or umbilicus (Cullens sign). Neither sign is pathognomonic of acute
pancreatitis; Cullens sign was first described in association with rupture of an ectopic
pregnancy. Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of
the legs.
Abdominal examination may reveal distension due to ileus or, more rarely, ascites with
shifting dullness. A mass can develop in the epigastrium due to inflammation. There is
usually muscle guarding in the upper abdomen, although marked rigidity is unusual. A pleural
effusion is present in 1020% of patients.
Pulmonary oedema and pneumonitis are also described and may give rise to the differential
diagnosis of pneumonia or myocardial infarction. The patient may be confused and exhibit the
signs of metabolic derangement together with hypoxaemia.
16
Investigations
Typically, the diagnosis is made on the basis of the clinical presentation and an elevated serum
amylase level. A serum amylase level three to four times above normal is indicative of the
disease.
A normal serum amylase level does not exclude acute pancreatitis, particularly if the patient has
presented a few days later. If the serum lipase level can be checked, it provides a slightly more
sensitive and specific test than amylase. If there is doubt, and other causes of acute abdomen
have to be excluded, contrast-enhanced CT is probably the best single imaging investigation.
Assessment of severity
On account of the difference in outcome between patients with mild and severe disease, it is
important to define that group of patients who will develop severe pancreatitis. Various scoring
systems have been introduced, such as the Ranson and Glasgow scoring systems.
The APACHE II scoring system, used in intensive care units, can also be applied. A severe
attack may be heralded by an initial clinical impression of a very ill patient and an APACHE II
score above 8. At 48 hours after the onset of symptoms, a Glasgow score of 3 or more, a C-
reactive protein level greater than 150 mg l1 and a worsening clinical state with sepsis or
persisting organ failure indicate a severe attack.
Severity stratification should be performed in all patients within 48 hours of diagnosis. Patients
with a body mass index over 30 are at higher risk of developing complications.
17
Imaging
Plain erect chest and abdominal radiographs are not diagnostic of acute pancreatitis, but are
useful in the differential diagnosis.
Non-specific findings in pancreatitis include a generalised or local ileus (sentinel loop), a colon
cut-off sign and a renal halo sign. Occasionally, calcified gallstones or pancreatic calcification
may be seen. A chest radiograph may show a pleural effusion and, in severe cases, a diffuse
alveolar interstitial shadowing may suggest acute respiratory distress syndrome.
Ultrasound does not establish a diagnosis of acute pancreatitis. The swollen pancreas may be
seen, but ultrasonography should be performed within 24 hours in all patients to detect gallstones
as a potential cause, rule out acute cholecystitis as a differential diagnosis and determine whether
the common bile duct is dilated.
CT is not necessary for all patients, particularly those deemed to have a mild attack on
prognostic criteria. But a contrastenhanced CT is indicated in the following situations:
if there is diagnostic uncertainty;
in patients with severe acute pancreatitis, to distinguish interstitial from necrotising

pancreatitis. In the first 72 hours, CT may underestimate the extent of necrosis. The severity of
pancreatitis detected on CT may be staged according to the Balthazar criteria;
in patients with organ failure, signs of sepsis or progressive clinical deterioration;
when a localised complication is suspected, such as fluid collection, pseudocyst or a

pseudoaneurysm.
Cross-sectional MRI can yield similar information to that obtained by CT. EUS and MRCP can
help in detecting stones in the common bile duct and directly assessing the pancreatic
parenchyma, but are not widely available. ERCP allows the identification and removal of stones
in the common bile duct in gallstone pancreatitis. In patients with severe acute gallstone
pancreatitis and signs of ongoing biliary obstruction and cholangitis, an urgent ERCP should be
sought.
The presentation is so variable that sometimes even an experienced clinician can be mistaken.
While this is not desirable, occasionally the diagnosis is only made at laparotomy. The
appearances at laparotomy are characteristic.
18
Management
If after initial assessment a patient is considered to have a mild attack of pancreatitis, a

conservative approach is indicated with intravenous fluid administration and frequent, but non-
invasive, observation. A brief period of fasting may be sensible in a patient who is nauseated and
in pain, but there is little physiological justification for keeping patients on a prolonged nil by
mouth regimen.
Antibiotics are not indicated. Apart from analgesics and anti-emetics, no drugs or interventions
are warranted, and CT scanning is unnecessary unless there is evidence of deterioration.
However, if a stable patient meets the prognostic criteria for a severe attack of pancreatitis, then
a more aggressive approach is required, with the patient being admitted to a high-dependency or
an intensive care unit and monitored invasively.
Patients with a severe attack should be admitted to an intensive care or high-dependency unit.
Adequate analgesia should be administered. Aggressive fluid resuscitation is important, guided
by frequent measurement of vital signs, urine output and central venous pressure. Supplemental
oxygen should be administered and serial arterial blood gas analysis performed. The haematocrit,
clotting profile, blood glucose and serum levels of calcium and magnesium should be closely
monitored.
A nasogastric tube is not essential but may be of value in patients with vomiting. Specific
treatments such as aprotinin, somatostatin analogues, platelet-activating factor inhibitors and
selective gut decontamination have failed to improve outcome in numerous clinical trials and
should not be given. There are no data to support a practice of resting the pancreas and feeding
only by the parenteral or nasojejunal routes. If nutritional support is felt to be necessary, enteral
nutrition (e.g. feeding via a nasogastric tube) is should be used.
There is some evidence to support the use of prophylactic antibiotics (intravenous cefuroxime, or
imipenem, or ciprofloxacin plus metronidazole) in patients with severe acute pancreatitis for the
prevention of local and other septic complications. The duration of antibiotic prophylaxis should
not exceed 14 days. Additional antibiotic use should be guided by microbiological cultures.
If gallstones are the cause of an attack of predicted or proven severe pancreatitis, or if the patient
has jaundice, cholangitis or a dilated common bile duct, urgent ERCP should be carried out
within 72 hours of the onset of symptoms. There is evidence that sphincterotomy and clearance
of the bile duct can reduce the incidence of infective complications in these patients. In patients
with cholangitis, sphincterotomy should be carried out or a biliary stent placed to drain the duct.
ERCP is an invasive procedure and carries a small risk of worsening the pancreatitis.
19
Complications of Acute Pancreatitis
a) Pseudocysts
Pseudocysts are sacs of fluid that can develop on the surface of the pancreas. They are a common
complication of acute pancreatitis and are thought to affect around 1 in 20 people with the
condition.
Pseudocysts usually develop four weeks after the symptoms of acute pancreatitis start. In many
cases, they do not cause any symptoms and are only detected during a computerised tomography
(CT) scan.
However, in some people pseudocysts can cause bloating, indigestion and a dull abdominal
(tummy) pain.
If the pseudocysts are small and not causing any symptoms, there may be no need for further
treatment as they usually go away on their own.
Treatment will usually be recommended if you are experiencing symptoms or if the pseudocysts
are large. Larger pseudocysts are at risk of bursting, which could cause internal bleeding or
trigger an infection.
Pseudocysts can be treated by draining the fluid out of the cyst by inserting a needle into it
through your skin. This can also be done by carrying out an endoscopy, where a thin, flexible
tube called an endoscope is passed down your throat and tiny tools are used to drain away the
fluid.
20
b) Infected pancreatic necrosis
In around one in three severe cases of acute pancreatitis, a common and serious complication
called infected pancreatic necrosis occurs.
In infected pancreatic necrosis, high levels of inflammation cause an interruption to the blood
supply of your pancreas. Without a consistent supply of blood, some of the tissue of your
pancreas will die. Necrosis is the medical term for the death of tissue.
The dead tissue is extremely vulnerable to infection from bacteria. Once an infection has
occurred, it can quickly spread into the blood (blood poisoning) and cause multiple organ failure.
If left untreated, infected pancreatic necrosis will almost certainly result in death.
Infected pancreatic necrosis usually develops two to six weeks after the symptoms of acute
pancreatitis started. It is marked by increased abdominal pain and a high temperature. The
infection will need to be treated with injections of antibiotics, and the dead tissue will need to be
removed to prevent the infection returning.
In some cases, it may be possible to drain away the dead tissue using a thin tube called a
catheter, which is placed through the skin.
Alternatively, laparoscopic surgery (keyhole surgery) can be used. A small cut is made in your
back and an endoscope is inserted to wash away any dead tissue.
It isn't always possible to use a laparoscopic approach in cases where an area of dead tissue is not
easily accessible, for example, or if you are obese. In such circumstances, a cut is made in your
abdomen to allow the dead tissue to be removed.
Infected pancreatic necrosis is a very serious complication. Even with the highest standards of
medical care the risk of dying from organ failure is estimated to be around one in five.
21
c) Systemic inflammatory response syndrome (SIRS)
Another common complication of severe acute pancreatitis is systemic inflammatory response

syndrome (SIRS). SIRS develops in an estimated 1 in 10 severe cases of acute pancreatitis.
In SIRS, the inflammation affecting the pancreas spreads throughout the body, which can cause
one or more organs to fail. It usually develops during the first week after the symptoms started,
with most cases developing on the same day.
Symptoms of SIRS include:
- a rise in body temperature to above 38C (100.4F) or a fall in body temperature to below 36C
(96.8F)
- a rapid heartbeat of more than 90 beats a minute
- an unusually fast breathing rate (more than 20 breaths a minute)
There is currently no cure for SIRS, so treatment involves trying to support the body's functions
until the inflammation has passed. The outcome depends on how many organs fail. The higher
the number of organs affected, the greater the risk of death.
Outcomes and follow-up of acute pancreatitis
The overall mortality from acute pancreatitis has remained at 1015% over the past 20 years.
There is a clear responsibility before the patient is discharged to determine the aetiology of the
attack of pancreatitis, and the causes must be looked for and excluded.
Failure to remove a predisposing factor could lead to a second attack of pancreatitis, which could
be fatal. A proportion of patients in the idiopathic group who suffer repeated attacks may prove
to have biliary microlithiasis, which can be identified only by bile sampling at ERCP or by
endoscopic ultrasound.
In a patient who has gallstone pancreatitis, the gallstones should be removed as soon as the
patient is fit to undergo surgery and, preferably, before discharge from hospital.
22
Patients review
Patient is a known case of acute pancreatitis since August 2013. He was admitted to the hospital
on 12th December 2013 due to recurrent acute pancreatitis and for this time it was worse
epigastric pain compared to the first episode. Patient is a student at SMK Pasir Puteh. Now, he is
in Form 3. After he was diagnosed with acute pancreatitis, his life totally changed.
This is because now he always have the discomfort over the abdomen. Sometimes he have to
take leave from school because of his illness. He have to cope with his illness and also with his
studies. He is lucky to have good teachers that concern about his condition. Now, he loss of his
appetite. Luckily, he has responsible parents that take good care of him. They always monitored
his health.
Patient said that this illness made his in trouble sometimes because he have to bear with the pain.
The pain usually come in a sudden onset. He is also happy with the way he is being treated in the
hospital as the doctors are treating him well.
He hope that he can get recover from this illness as he is still young. He also hope that this
illness do not interfere with his life and he wants to live as a normal boy like everyone else.
Other than that, he will not give up no matter how serious is his illness and he prays that he can
recover as soon as possible.
23
REFERENCES
1. Bailey & Loves Short Practice of Surgery 24th Edition, Norman S. Williams, Christopher
J.K. Bulstrode, P. Ronan OConnell.
2. Surgery : an Oxford Core Text, Peter Stonebridge, David Smith, Lesley Duncan, Alastair
Thompson
24
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Rasyidah binti Rustam | 57260211004

Year 3 MBBS UniKL/VMU | 2011/2016

UNIVERSITI KUALA LUMPUR (UNIKL)

Name : Rasyidah binti Rustam

Address : Pasir Puteh, Ipoh

Marital status : Single

Hospital registration no. : HRPB 5200516

NRC no. : 980618-08-6325

Date of admission : 12th December 2013

Date of clerking : 15th December 2013

Date of discharge : 16th December 2013

Abdominal pain three days prior to admission.

History of presenting illness

Respiratory system No difficulty in breathing, no cough, no

Past medical history

Past surgical history

Patient is on T. Lovastatin 20mg. He is not compliance to the drugs.

There is no known drugs, food and environment allergy.

There were no lymph nodes enlargement, no swelling, no thyroid enlargement and no

There was no pitting edema.

Liver : The liver was not palpable.

Spleen : The spleen was not palpable.

Spleen : Traubes space was resonant, no splenomegaly.

There was no shifting dullness and no fluid thrill.

Per rectal examination

Acute mesentric ischemia

Full blood count (FBC)

Patients value Normal value Interpretation

Patients Value Normal Value Interpretation

Urine diastase test

Patients Value Normal Value Interpretation

Patients Value Normal Value Interpretation

Liver Function Test (LFT)

Patients value Normal value Interpretation

NORMAL RANGE RESULT

Arterial Blood Gas (ABG)

Patients value Normal value Interpretation

Chest Xray (CXR)

Result: no free intraperitoneal air, lung field are clear, no cardiomegaly.

Abdomen Xray (AXR)

Result: no dilated bowels, no gallstones, Riglers sign is negative.

Recurrent acute pancreatitis.

Daily progress of the patient

12th December 2013

Respiratory rate: 20 breaths per minute

Blood pressure: 136/79 mmHg

13th December 2013

Pulse: 90 beats per minute, regular rhythm and good volume

Respiratory rate: 20 breaths per minute

Blood pressure: 128/78 mmHg

14th December 2013

Pulse : 96 beats per minute, regular rhythm and good volume

Respiratory rate: 20 breaths per minute

Blood pressure: 119/60 mmHg

15th December 2013

Pulse: 98 beats per minute, regular rhythm and good volume

Respiratory rate: 20 breaths per minute

Blood pressure: 119/83 mmHg

16th December 2013

Respiratory rate: 20 breaths per minute

Blood pressure: 135/78 mmHg

The underlying mechanism of injury in pancreatitis is thought to be premature activation of

Acute pancreatitis may be categorised as mild or severe. Mild acute pancreatitis is

Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas