SURGERY

ANN CHEW LIYEN

1001129434
Year 3, Group 3
20th June 2016
HISTORY
Personal Identification

Name: Mohd Hisyamuddin b. Muhammad

Age: 24 years old

Gender: Male

Ethnic: Malay

Religion: Muslim

Address: Batu Enam

Occupation: Manual labor in electrical wiring

Date of admission: 13th June 2016

Date of clerking: 19th June 2016

Place: Hospital Sultanah Nur Zahirah (HSNZ)

Presenting Complaints

Sudden severe upper abdominal pain 1 hour before admission.

History of Presenting Illness

Patient was apparently well until the day of admission after he broke fast in the evening. He was
resting when there was sudden severe epigastric pain 45 minutes after his meal. He had chicken rice,
iced cordial and some pastries, not particularly oily food. The pain was boring in nature, continuous
and increased in intensity from the initial 8/10 on the pain score to 10/10 before admission. It was so
severe he could hardly stand. There was no radiation to the back. It was aggravated with inspiration
and was relieved slightly by leaning forwards. This is the first time he has experienced this type of
pain.

There was also abdominal distension, and he reported it as being tense and bloated. The episode was
also associated with profuse sweating and nausea. He was brought to HSNZ emergency department by
his brother and was admitted into the ward where he vomited once. The vomitus contained food
residue and there was no blood among it. The pain was not relieved by vomiting.

He was given analgesics and the pain subsided. He was also given anti-emetics and IV potassium
chloride. 2 ultrasound scans were done that revealed multiple small gallstones.

Patient admitted to chronic use of a traditional medicine i.e. ‘ubat manjong’ to help relieve his
occasional muscle pain. He takes it whenever he has severe muscle pain, usually once or twice a week.
The medication may be steroidal or a NSAID in nature, but cannot be confirmed. He is also a chronic
smoker for the past 7 years, around a pack a day. He is usually able to tolerate fatty food.
Patient denied having any fever, steatorrhea, dark stools, pale urine, pruritus or change in frequency of
urination and bowel emptying. There was no water brash, odynophagia or dysphagia. No aneroxia or
loss of weight. No hematemesis or melena.

Systemic Review

Genitourinary  No incontinence, change in frequency, dysuria, or

hematuria.
Cardiovascular System  No chest pain, palpitations.
 No dyspnea, orthopnea, or paroxysmal nocturnal dyspnea.
Respiratory System  No shortness of breath, cough, or abnormal breath sounds.
Nervous System  No headaches, seizures, altered body movement, tremors,
or focal neurological deficit.
Musculoskeletal  No muscle or join pain, stiffness, or swellings.
 No abnormal posture or recent gait changes.

Past History

Patient had acute appendicitis in 2010, appendectomy was done with no complications or sequelae.

He had no other previous hospitalisations or operations done, and doesn’t suffer from any chronic
illness.

Drug History

Patient is not taking any medications currently. Besides the ‘ubat manjong’, he denied taking any other
traditional and herbal drugs, chronic use of over-the-counter drugs, vitamins or supplements.

He is not known to be allergic to any medication or food.

Family History

Patient’s mother suffers from diabetes and hypertension. His siblings and father do not have any
known chronic medical illnesses.

There are no similar problems, liver diseases, jaundice or malignancy in his family.

Social and Personal History

Patient is single and stays with his family at Batu Enam in a kampong house which has proper
amenities.

He works as a manual labourer in electrical wiring which requires heavy lifting. He is a chronic
smoker for the past 7 years and smokes about a pack a day. He denied consuming any alcohol or
recreational drugs. He has a balanced diet consisting mainly of rice and seafood, and can tolerate fatty
food.
PHYSICAL EXAMINATION

General Appearance

Patient was conscious, co-operative and orientated to time, place and people. He is of moderate build,
and seemed to be well-nourished and hydrated. He was not in pain or respiratory distress.

Vital Signs

Pulse rate 96/min, regular rhythm, normal volume

Respiratory rate 20/min (normal)
Blood pressure 118/76mmHg (normotensive)
Temperature 37 o C (afebrile)
Pain None

General Examination

On examination of head, there was sclera icterus. No pallor. Oral hygiene is fair, no signs of central
cyanosis or aphthous ulcers, no fetor hepaticus.

There were no swellings, skin changes or palpable lymph nodes in the neck. JVP was not raised, no
visible pulsations. No tracheal deviation.

The hands were dry and warm. No signs of clubbing, palmar erythema, fine or flapping tremors,
Dupuytren’s contracture or peripheral cyanosis. No koilonychia, leukonychia or nicotin-staining.
Capillary refill time was normal (less than 2 seconds).

There were no scratch marks, skin changes, signs of varicose veins or pitting edema on both lower
limbs. Capillary refill time was normal.

Local Examination

Abdomen

Inspection  Abdomen is flat and moves symmetrically with respiration.

 Umbilicus is inverted and centrally located.
 Normal skin color of abdomen, no visible scars or stomas,
peristalsis, or pulsations. No caput medusae.
 No Grey-Turner’s, Cullen’s, Fox’s or Murphy’s signs.
Palpation  Abdomen is soft, non-tender and normal in temperature.
 No muscle guarding or rigidity.
 No palpable mass. No hepatomegaly, splenomegaly, kidneys
not ballotable.
Percussion  Normal resonant percussion notes.
 Shifting dullness and fluid thrill negative.
Auscultation  Normal bowel sounds, 2 times per minute, normal pitch.
 No aortic or renal bruits, no venous hum.
Systemic Examination

Chest

Inspection  Chest shape is normal and moves symmetrically with

respiration.
 No chest deformities, visible scars, pulsations, or dilated
veins.
 No spider naevi, gynecomastia.
Palpation  Chest expansion equal and symmetrical on both sides in all 3
zones.
 Apex beat is felt at 5th intercostal space, midclavicular line.
 No thrills or right ventricular heave.
 Vocal fremitus was normal.
Percussion  Normal resonance in all 3 zones.
Auscultation  Air entry is equal on both sides, normal vesicular breath
sounds with no added breath sounds.
 Both S1 and S2 are heard and normal with no additional heart
sounds.
 No pleural rub.
 No basal crepitations or sacral edema.

Neurological

Patient was alert, conscious and orientated to time, space and person. His higher brain function was
normal, memory was intact. Cranial nerves, motor, and sensory system were also intact. He was able
to move all 4 limbs independently without difficulty, has ormal posture and gait with good muscle
coordination.

SUMMARY

24-year-old Malay male presenting with sudden severe boring epigastric pain 45 minutes post-prandial
with no radiation to the back. It was continuous and increased in intensity, was aggravated by
inspiration and slightly relieved by leaning forward. It was associated with abdominal distension,
profuse sweating, nausea and vomiting. Physical examination revealed sclera icterus. Ultrasound scans
revealed gallstones.

Patient is also a chronic smoker for 7 years and taking a traditional medicine of unknown classification
for muscle pain relief, and could tolerate fatty food normally.

PROVISIONAL DIAGNOSIS
Acute pancreatitis secondary to gallstones

Points for:

 Sudden severe epigastric pain

 Boring pain
 Pain aggravated by inspiration, relieved slightly by leaning forward
 Associated nausea and vomiting
 Scleral icterus
 Gallstones found upon ultrasound scans

Point’s against:

 Pain doesn’t radiate through or around to the back.

DIFFERENTIAL DIAGNOSIS

Disease Points for Points against

Ascending  Sudden epigastric pain  Pain doesn’t localise to right
cholangitis  Severe upper quadrant.
secondary to  Nausea and vomiting  No fever
choledocholithiasi  Scleral icterus
s
Peptic ulcer  Sudden epigastric pain  Vomiting doesn’t relieve pain
 Post-prandial pain  No hematemesis or melena.
 Chronic smoker
 Possible
steroid/NSAID use
(chronic use of
unknown traditional
medicine)
Gastroesophageal  Sudden epigastric pain  Scleral icterus present.
reflux disease  Post-prandial pain  No water brash
(GERD)  Np dysphagia, odynophagia

INVESTIGATIONS

1. Serum amylase and lipase – both will increase in acute pancreatitis; serum amylase
diagnostic if 3 times beyond normal, >1000IU/ml.
2. Urine amylase – is elevated in acute pancreatitis. Used to differentiate between increased
serum amylase due to acute pancreatitis or macroamylasemia. Can be used if patient presents
several days after abdominal pain (serum lipase usually not done because it’s expensive)
3. Liver function test – increased AST and LDH, decreased serum albumin in acute pancreatitis.
Increased ALP and bilirubin level in obstructive jaundice.
 4. BUSE creatinine – serum urea and creatinine levels increase due to 3 rd space loss. Calcium
might be low due to saponification.
5. Full blood count – increased WBC count indicating infection. Also one of Ranson’s criteria
used in acute pancreatitis.
6. Blood sugar level – acute pancreatitis may lead to hyperglycemia.
7. ABG – pH may decrease. Respiratory distress, pulmonary edema, metabolic or respiratory
acidosis may occur.
8. Coagulation profile
9. Transabdominal ultrasound – check for dilatation of common bile duct, gallstones.
Pancreatic swelling with peripancreatic fluid accumulation and edema in pancreatitis.
Thickened gallbladder wall in acute cholecystitis.
10. ERCP – visualise pancreatic and biliary duct.
11. Abdominal X-ray – to exclude other causes of acute abdomen. Erect X-ray for
pneumoperitoneum, supine for adhesion colic or dilated small bowels. In acute pancreatitis,
colon cut off sign might be seen.
12. Esophago-gastro-duodenoscopy – exclude gastritis, peptic ulcer and esophagitis.
13. Chest X-ray – to check for atelactasis and pleural effusion in acute pancreatitis.

MANAGEMENT

Conservative
1. Nil by mouth as there may be paralytic ileus and at the same time reduce pancreatic juice
secretion stimulation.
2. IVF dextrose for nutritional support.
3. Pain relief – opoids instead of NSAIDs because patient is given pain relief before confirmation
of diagnosis. Giving NSAIDs will exacerbate peptic ulcers.
4. Antiemetics to stop vomiting
5. Nasogastric tube if there’s persistent vomiting to decompress stomach.
6. Calcium and magnesium therapy if disease is severe.
7. Oxygen supplement as patient might have respiratory distress. The most common COD in
acute pancreatitis in the 1st week is ARDS.
8. Input output chart to monitor hypovolemia due to 3rd space loss.
9. Monitor vital signs 4-hourly.

Endoscopic treatment
Endocopic retrieval of stone from biliary tree using a basket or balloon following endoscopic
sphincterotomy.

Surgical treatment
Associated with gallstones
1. Laproscopic cholecystectomy to remove stone. Laproscopic surgery is preferred over open
surgery as it causes less tissue trauma, pain, morbidity, hospital-acquired infections, risks of
deep vein thrombosis and has an shorter recovery period.
2. ERCP
Other causes
1. If pancreatic duct system is distended, perform pancreaticojejunostomy for drainage.
2. If drainage is not feasible (the duct system is not distended), perform resection of pancreas.
Distal pancreatectomy is done if the distal gland is involved. Pacreaticoduodenectomy is done
Whipple procedure of the head of gland is involved

DISCUSSION

The pancreas lies retroperitoneally, behind the lesser sac and stomach. The head of the gland lies
within the C-loop of the duodenum, with which it shares a blood supply from the coeliac and superior
mesenteric arteries. The superior mesenteric vein runs upwards to the left of the uncinate process, and
joins the splenic vein behind the neck of the pancreas to form the portal vein. The body and tail of the
pancreas lie in front of the splenic vein as far as the splenic hilum, and receive arterial blood from the
splenic artery as it runs along the upper border of the gland.

The intimate relationship of the friable pancreas to these major blood vessels is the reason that
bleeding is problematic after pancreatic trauma. The close association between the common bile duct
and the head of pancreas explains why obstructive jaundice is so common in cancer of the head of the
pancreas, and why gallstones frequently give rise to acute pancreatitis.

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 a
prolonged and frequently lifelong disorder resulting from the development of fibrosis within the
pancreas. It is probable that acute pancreatitis is but a phase of chronic pancreatitis.

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. It may be caused by obstruction of the pancreatic duct,
usually by a small gallstone obstructing the ampulla of Vater. Hypercalcaemia is a rare cause of
pancreatitis and is usually secondary to hyperparathyroidism. Hyperlipidaemia, due to familial
hypertriglyceridaemia, is another rare cause of pancreatitis and in both of these metabolic conditions
treatment is directed at the underlying cause.

A small number of patients may have a family history of acute pancreatitis. Hereditary pancreatitis is a
rare condition caused by mutations of the cationic trypsinogen gene and leads to the development of
chronic pancreatitis at a young age. Viral infections, including mumps, Coxsackie virus, rubella,
measles and cytomegalovirus are the most common cause of pancreatitis in children. Bacterial
infections are a very rare cause of pancreatitis. Ascaris worms are a relatively common cause of
pancreatitis in areas of high prevalence, due to migration through the duodenal papilla from the
common bile duct.

Many drugs have been associated with acute pancreatitis although it is often difficult to prove a causal
association and other causes always need to be considered. Azathioprine, mesalazine and simvastatin
are responsible for the best documented cases. Pancreatic neoplasms may cause obstruction of the
pancreatic duct and lead to acute pancreatitis. Such neoplasms can be small and thus easily missed,
even by CT. The presence of unexplained pancreatic duct dilatation or other suspicious clinical or
radiological appearances should prompt further investigation, usually by endoscopic ultrasound.

Pancreatitis is equally common in males and females. The peak incidence is in the fourth and fifth
decades of life, but it can occur at any ages. The common presenting symptom is pain that begins
suddenly and high in the epigastrium, and steadily increases in severity until it is very severe, causing
the patient to lie still and breathe shallowly. It usually radiates through to the back. Pain is exacerbated
by movement and is relieved by leaning forward. Frequent vomiting and retching are very common.
There is persistent nausea between the bouts of vomiting. In this patient, he had quite a classic
presentation of acute pancreatitis in such that he had sudden onset of severe epigastric pain which
radiates to the back and is relieved by leaning forward.

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 l–1 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.

Ranson’s prognostic criteria

On admission:
• Old age >55 years
• Blood sugar >200 mg%
• TC >16,000/mm3
• Serum LDH > 350 IU/L
• Serum SGOT > 250 IU/L

In 48 hrs:
• Base deficit > 4 mEq/L
• Serum calcium < 8 mEq/L
• Haematocrit : altered by 10%
• Arterial O2 (PO2) < 60 mm Hg
• Extravascular space fluid loss: > 6 L
• Blood urea (BUN) altered > 5 mg% of the normal

Total score is 11
Scores up to 5 — better prognosis
5-7 — equivocal—but dangerous
>7 — is highly dangerous
Glasgow criteria
• Age > 55 years
• PO2 < 8 KPa
• Total count >15000 cells/mm3
• Serum calcium < 2 mmoles/L
• Blood urea > 16 mmol/L
• Blood glucose > 10 mmols/L (200 mg%, no
H/O diabetes)
• SGPT > 200 IU/L
• LDH > 600 U/L
• Serum albumin < 3.2 gm/dl

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. 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.

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.

Pancreatitis may involve all organ systems and place demands on the surgeon beyond his or her skills.
Patients with systemic complications should be managed by a multidisciplinary team that includes
intensive care specialists. When there is organ failure, appropriate supportive therapies may include
inotropic support for haemodynamic instability, haemofiltration in the event of renal failure,
ventilatory support for respiratory failure and correction of coagulopathies (including DIC). There is
no role for surgery during the initial period of resuscitation and stabilisation; surgical intervention is
contemplated only in the patient who deteriorates as a result of local complications following
successful stabilisation.

Late deaths are usually due to complications arising from infected pancreatic necrosis, with mesenteric
ischaemia or severe retroperitoneal bleeding being common terminal events. Following recovery from
severe acute pancreatitis, return to normal activities can be expected but full recovery can take many
months, requiring nutritional support, management of persistent or recurrent sepsis and definitive
management of wound or gastrointestinal complications.