ACUTE PANCREATITIS

2. CASE PRESENTATION
By:
Dr. ZULAIKHA MALIK
PGR WMW

3. BIODATA
 NAME: SHAHID
 AGE: 33yrs
 SEX: male
 MARITAL STATUS: single
 RESIDENT OF: KAREEM PARK,lahore
 OCCUPATION: tailor
 D.O.A. : 25/10/14
 M.O.A. : ER

4. PRESENTING COMPLAINTS
 FEVER 7 DAYS
 VOMITING 3 DAYS
OLIGURIA 2 DAYS
YELLOW DISCOLRATION OF SCLERA 2
DAYS

5. HOPI
My patient was in his usoh 7 days back when he started having fever
that was acute,continuous,high grade,with rigors and chills,relieved
temporarily by medication .
There is no h/o cough/sputum, burning micturition,diarrhoea,joint
pains,jaundice,SOB.
Patient had c/o vomiting for 3 days which was acute,non
bilious,projectile,contained food particles and started even with a
sip of water.
Pt c/o decreased urine for the last 2 days
Pt c/o yellow discolration of sclera for 2 days

6. HOPI contd:
There is no h/o cough,sputum,hemoptysis or wheeze or
allergies.no h/o tb contact
 No h/o orthopnea,PND,pedal edema.palpitations, chest
pain.
 There is no h/o dizzines,blackouts,headache,tingling,
numbness or weakness of any side of the body No
history of chest pain, palpitations, syncope, orthopnea,
PND or pedal edema..
 No history of abdominal pain, diarrhea, constipation,
vomitting,urinary frequency,urgency,burning
micturation or any genital ulcers..
 No history of difficulty standing from sitting posture

7. HISTORY CONTINUED..
 PAST HISTORY: no history of hospital admission
for any complaint
 SURGICAL HISTORY: insignificant
 DRUG HISTORY: pt was a non smoker non
addict .h/o iv drug abuse was negative.
 NO H/O EXPOSURE TO RAT S
 PERSONAL HISTORY:non diabetic,non
hypertensive,non-smoker.no h/o IHD
 FAMILY HISTORY:insignificant .
 SOCIO-ECONOMIC: belongs to middle class..

9. 1.ACUTE PANCREATITIS
2.ACUTE GASTRITIS
3.ACUTE HEPATITIS
4.LEPTOSPIROSIS
5.AKI DUE TO UROSEPSIS

10. EXAMINATION
A young male of average height and built,lying in bed,
with branula over His right hand having following vitals:
 PULSE: 110/min
 B.P. : 170/90 mmHg
 TEMP: Afebrile
 R/R: 16/min

11. GPE:
 PALLOR ++
 Jaundice +
 PEDAL EDEMA+
 FACIALPUFFINESS +
 GENERALIZED BODY SWELLING +
 RIGHT PAROTID SWELLING +
 CYANOSIS –
 JVP.NOT RAISED
 LYMPHADENOPATHY –


12. SYSTEMIC REVIEW
GIT
inspection
abdomen scaphoid, normal pattern of hair
distribution,no striae, scar mark or visible
pulsations,normal pattern of breathing,hernial
orifices intact.no bruises or discoloration around
umbilicus (cullen’s sign negative).no bruises in flanks
(grey turner sign negative)

13. PALPATION:
Superficial palpation: unremarkable
 DEEP PALPATION:
 abdomen is tender all over especially in
the epig region.
 no mass palpable
 no visceromegaly
 b/s audible(2sets/min)

14. PERCUSSION:
 FLUID THRILL –
 FLANK DULLNESS –
AUSCULTATION:
 BS ++

15. CNS :
GCS 11/15..
HMF,CN:intact
SOMI –
PUPILS B/L REACTIVE
PLANTARS B/L MUTE
SENSORY SYSTEM: couldn’t be assessed PROPERLY
BUT WITHDRAWS ON PAINFUL STIMULUS
MOTOR:normal bulk,tone,power and reflexes,both
upper limbs and lower limbs
FUNDOSCOPY:normal

16. CVS :
 INSPECTION:No visible pulsations,striae or
scar mark
 APEX BEAT:in 5th ICS,midclavicular line.
 S1+S2:of normal intensity and character with
no added sound
 No pericardial rub

17. RESP:
No chest deformity with thoraco-abdominal
breathing pattern
 Trachea central
 Chest expansion:4cm
 Normal vocal fremitus bilaterally
 Auscultation:NVB with bilateral equal air
entry .no added sounds,normal vocal
resonance,no pleural rub..

18. CASE SUMMARY
 a young male with h/o continuous high grade fever with
rigors and chills for 7 days and projectile vomiting for 7
days with no h/o asoc.and jaundice for 2 days.
 on examination he is drowsy but responsive,has
tachycardia,hypertension, tender abdomen,b/l pitting
pedal edema,oliguria but no dysuria or hematuria or pain
in flanks

20.  ACUTE PANCREATITIS
 AKI DUE TO UTI
 LEPTOSPIROSIS
 ACUTE HEPATITIS

21. PROGRESS
25/10
At admission
26/1
0
27/10
AFTER
48 HRS
28/
10
29/10 30/10 31/10
HB 14
TLC 34 12.5
UREA 88 92
CREAT 6 7 9 11 11.9 13
AMYLASE 273 161 352
LIPASE 103 323 218
LDH 370 808 1103
CA 7 7 7.2
ALT/AST 158/294 746/27
6
450/85

22. 26/10 28/10 30/10
ABG’S PH 7.34
PO2
PCO2 27
HCO3 15
02 SAT 92%
PH 7.36
PO2
PCO2 27
HCO3 16
O2 SAT
CKMB/CKNAC 266/110 60/125
NA/K 132/4.2 135/5.8 133/5.3
PT/APTT 19/33
TG
452
HDL
32
CHOL
185
BIL
DIRECT BIL
INDIRECT BIL
1.1 9
5.9
3.2

23. LABS
HEP C
HEP B
HIV BY KIT
HIV BY ELISA
URINE
COMPLETE
NEGATIVE
NEGATIVE
WEAKLY
POSITIVE
NEGATIVE
PUS CELLS 8-
10
BLOOD -
GLUCOSE -
KETONES NIL
PROTEIN +2

24. FURTHER PLAN :
 LEPTOSPIRAL ANTIBODIES WERE AWAITED
 Ct brain plain
 Ct contrast abdomen
 Mri abdomen
 Gamma GT

25.  CXR: NORMAL
 USGAbd: fatty liver
 ECG: SINUS TACHYCARDIA

26. CXR:
 NOT AVAILABLE

27. ECG

28. FINAL DIAGNOSIS
ACUTE PANCREATITIS

29. TREATMENT GIVEN IN WARD
INJ MERONEM 5OOMG IV BD
INJ FLAGYL 500MG IV TDS
INJ ISOKET @ 30 DPM
INJ RISEK 40MG IV BD
INJ LASIX 60MG IV BD
INJ CA GLUCONATE IV TDS
INF N/S 1000CC IV OD
INF 5% D/W 1000ML +1AMP HEPAMERZ IV BD
INJ METOMIDE IV TDS
INJ TRANSAMINE 250MG IV TDS
INJ AMINOVIL 500ML IV OD
INJ TANZO 2.25G IV TDS
INJ OXIDIL 1G IV BD
TAB MINIPRESS 1MG PO TDS
TAB NORVASC 10MG PO OD

30. STAT ORDERS
 INJ SOLUCORTEF 250MG STAT
 INJ HYDRALAZINE20MG IV IN 100ML N/S
OVER 15 MIN
 INJ AMINOVIL 500MG IV OD
 DUPHALAC ENEMA STAT
 INJ OXIDIL 1D IV BD

31. TREATMENT IN THE HDU:
TREATMENT OF UNCONTROLLED HYPERTENSION
IOP MONITORING
ANTIBIOTIC PROPHYLAXIS
TERMINAL EVENTS:
PT DETERIORATED BY DAY 5 .DEC IN URINE
OUTPUT.PLAN FOR HD WAS MADE.PT WENT FOR IST
SESSION OF HD BUT COULD NOT MAKE IT.PT HAD
UNCONTROLLED HYPERTENSION.PT COLLAPSED AT
THE START OF THE DIALYSIS SESSION AND BSL WAS
48.HE WAS BPLESS AND PULSELESS.HE WAS
IMMEDIATELY SENT TO EMERGENCY ICU .CPR WAS
DONE AND PT WAS RESUSCITATED BUT OF NO AVAIL.

32. COMPLICATIONS OF DIALYSIS:
 Hypotension
 A decrease in blood pressure is the most frequent complication reported
during hemodialysis. When fluid is removed during hemodialysis, the
osmotic pressure is increased and this prompts refilling from the
interstitial space. The interstitial space is then refilled by fluid from the
intracellular space. Excessive ultrafiltration with inadequate vascular
refilling plays a major role in dialysis induced hypotension. The
immediate treatment to hypotension is to discontinue dialysis and place
the patient in a trendelenburg position. This will increase cardiac filling
and may increase the blood pressure promptly.
 Cramps
 In the majority of hemodialysis patients, cramps occur toward the end of
the dialysis procedure after a significant volume of fluid has been
removed by ultrafiltration. The immediate treatment for cramps is
directed at restoring intravascular volume through the use of small
boluses of isotonic saline. Prevention of cramps has been attempted
with the prophylactic use of quinine sulfate at least 2 hours prior to
dialysis.

33.  Arrhythmia
 Patients on maintenance hemodialysis are at risk of cardiac
arrhythmias. They occur predominately in association with
hemodialysis or may occur in the interdialytic period. Both
acute and chronic alterations in fluid, electrolyte, and acid-base
homeostasis may be arrhythmogenic in these
patients.
 Hemolysis
 Hemolysis may result from a number of biochemical and
toxic insults during the dialysis procedure. The half-life of
red blood cells in renal failure patients is approximately one
half to one third of normal and the cells are particularly
susceptible to membrane injury.

34. Febrile reactions
Febrile episodes should be aggressively evaluated with appropriate wound and
blood cultures. The suspicion of infection should be high. Treatment of
endotoxin related fever is generally supportive with antipyretics. Temperatures
should be recorded at the initiation and termination of dialysis treatment.
Hypoxemia
A fall in arterial PO2 is a frequent complication of hemodialysis that occurs in
nearly 90% of patients. The drop ranges from 5 to 35 mm Hg, and reaches its
peak between 30 - 60 minutes after beginning dialysis. This is obviously
undesirable for patients with underlying cardiopulmonary disease. Also,
patients on mechanical ventilators with constant minute volume and inspired
oxygen concentration can still develop hypoxemia during hemodialysis.

35. ACUTE
PANCREATITIS

36. ACUTE PANC
 Acute pancreatitis or acute pancreatic
necrosis[1] is a sudden inflammation of the
pancreas. It can have severe complications and
high mortality despite treatment. While mild
cases are often successfully treated with
conservative measures, such as NPO (nil per os,
fasting) and aggressive intravenous fluid
rehydration, severe cases may require
admission to the intensive care unit or even
surgery to deal with complications of the
disease proces

38. S/S
The most common symptoms and signs include:
 severe epigastric pain (upper abdominal pain)
radiating to the back,severe,boring,gets worse
on lying supine and walking.
 nausea
 vomiting
 loss of appetite
 Fever
 chills (shivering)
 hemodynamic instability, which include shock
 tachycardia (rapid heartbeat)
 respiratory distress
 peritonitis

39. LESS COMMON SIGNS
 Signs which are less common, and indicate severe disease,
include:
 Grey-Turner's sign (hemorrhagic discoloration of the
flanks)
 Cullen's sign (hemorrhagic discoloration of the umbilicus)
 Pleural effusions (fluid in the bases of the pleural cavity)
 Grünwald sign (appearance of ecchymosis, large bruise,
around the umbilicus due to local toxic lesion of the
vessels)
 Körte's sign (pain or resistance in the zone where the head
of pancreas is located (in epigastrium, 6–7 cm above the
umbilicus))
 Kamenchik's sign (pain with pressure under the xiphoid
process)
 Mayo-Robson's sign (pain while pressing at the top of the
angle lateral to the Erector spinae muscles and below the
left 12th rib (left costovertebral angle (CVA))[2]

41. CAUSES
 Most common causes
 Alcohol
 Gallstones
 Metabolic disorders: hereditary pancreatitis, hypercalcemia,
hyperlipidemia, malnutrition
 ERCP
 Abdominal trauma
 Penetrating ulcers
 Carcinoma of the head of pancreas, and other cancer
 Drugs: diuretics (e.g., thiazides, furosemide), gliptins e.g.,
vildagliptin, sitagliptin, saxagliptin, linagliptin, tetracycline,
sulfonamides, estrogens, azathioprine and mercaptopurine,
pentamidine, salicylates, steroids[citation needed]
 Infections: mumps, viral hepatitis, coxsackievirus,
cytomegalovirus, Mycoplasma pneumoniae, Ascaris
 Structural abnormalities: choledochocele, pancreas divisum
 Radiation X-ray

42. Assessment of severity:
 RANSON CRITERIA
 SOFA SCORE
 APACHE 2 SCORE

43. BISAP SCORE:
 Used to assess the sverity in the first 24 hrs at
the bedside.IT IS USED TO IDENTIFY PTS AT
RISK OF MORTALITY
 BUN> 25(THE RATE OF INC IN BUN IS
PROPORTIONATE TO THE RISK FOR
MORTALITY)
impaired mental status
SIRS
AGE>60
PLEURAL EFFUSION

44. PATHOGENESIS
In mild pancreatitis
there is inflammation and edema of the pancreas.
In severe pancreatitis there are additional features of necrosis and secondary
injury to extrapancreatic organs. Both types share a common mechanism of
abnormal inhibition of secretion of zymogens and inappropriate activation of
pancreatic zymogens inside the pancreas, most notably trypsinogen. Normally,
trypsinogen is activated to trypsin in the duodenum where it assists in the
digestion of proteins. During an acute pancreatitis episode there is colocalization
of lysosomal enzymes, specifically cathepsin, with trypsinogen. Cathepsin
activates trypsinogen to trypsin leading to further activation of other molecules
of trypsinogen and immediate pancreatic cell death according to either the
necrosis or apoptosis mechanism (or a mix between the two). The balance
between these two processes is mediated by caspases which regulate apoptosis
and have important anti-necrosis functions during pancreatitis: preventing
trypsinogen activation, preventing ATP depletion through inhibiting polyADP-ribose
polymerase, and by inhibiting the inhibitors of apoptosis (IAPs). If,
however, the caspases are depleted due to either chronic ethanol exposure or
through a severe insult then necrosis can predominate.

45.  As part of the initial injury there is an extensive
inflammatory response due to pancreatic cells
synthesizing and secreting inflammatory
mediators: primarily TNF-alpha and IL-1. A
hallmark of acute pancreatitis is a manifestation
of the inflammatory response, namely the
recruitment of neutrophils to the pancreas. The
inflammatory response leads to the secondary
manifestations of pancreatitis: hypovolemia
from capillary permeability, acute respiratory
distress syndrome, disseminated intravascular
coagulations, renal failure, cardiovascular failure,
and gastrointestinal hemorrhage

46. DIAGNOSIS
 Acute pancreatitis is diagnosed clinically but requires
CT evaluation to differentiate mild acute pancreatitis
from severe necrotic pancreatitis. Experienced
clinicians were able to detect severe pancreatitis in
approximately 34-39% of patients who later had
imaging confirmed severe necrotic pancreatitis.
Blood studies are used to identify organ failure, offer
prognostic information, determine if fluid
resuscitation is adequate, and if antibiotics are
indicated.
 ]

47. BLOOD INVESTIGATIONS
Full blood count,
Renal function tests,
Liver Function,
serum calcium,
serum amylase and lipase,
Arterial blood gas,
Trypsin-Selective Test[7

48. GOLD STANDARD INVESTIGATION
 Imaging - A triple phase abdominal CT and
abdominal ultrasound are together
considered the gold standard for the
evaluation of acute pancreatitis. Other
modalities including the abdominal xray lack
sensitivity and are not recommended. An
important caveat is that imaging during the
first 12 hours may be falsely reassuring as the
inflammatory and necrotic process usually
requires 48 hours to fully manifest.

49.  Labs
 Elevated serum amylase and lipase levels, in combination with severe
abdominal pain, often trigger the initial diagnosis of acute pancreatitis.
However, they have no role in assessing disease severity.
 Serum lipase rises 4 to 8 hours from the onset of symptoms and
normalizes within 7 to 14 days after treatment.
 Serum amylase may be normal (in 10% of cases) for cases of acute or
chronic pancreatitis (depleted acinar cell mass) and
hypertriglyceridemia.
 Reasons for false positive elevated serum amylase include salivary gland
disease (elevated salivary amylase), bowel obstruction, infarction,
cholecystitis, and a perforated ulcer.
 If the lipase level is about 2.5 to 3 times that of amylase, it is an
indication of pancreatitis due to alcohol.[8]
 Decreased serum calcium
 Glycosuria

50. COMPUTED TOMOGRAPHY
 CT is an important common initial assessment tool for
acute pancreatitis. Imaging is indicated during the initial
presentation if:
 the diagnosis of acute pancreatitis is uncertain
 there is abdominal distension and tenderness, fever>102, or
leukocytosis
 there is a Ranson score > 3 or APACHE score > 8
 there is no improvement after 72 hours of conservative
medical therapy
 there has been an acute change in status: fever, pain, or
shock

51. MRI:
 While computed tomography is considered the gold
standard in diagnostic imaging for acute
pancreatitis,[14] magnetic resonance imaging (MRI)
has become increasingly valuable as a tool for the
visualization of the pancreas, particularly of
pancreatic fluid collections and necrotized debris.[15]
Additional utility of MRI includes its indication for
imaging of patients with an allergy to CT's contrast
material, and an overall greater sensitivity to
hemorrhage, vascular complications,
pseudoaneurysms, and venous thrombosis.[16]

52. RANSON SCORE
Ranson criteria is a clinical prediction rule for
predicting the severity of acute pancreatitis. It was
introduced in 1974.[1]
At admission
 age in years > 55 years
 white blood cell count > 16000 cells/mm3
 blood glucose > 10 mmol/L (> 200 mg/dL)
 serum AST > 250 IU/L
 serum LDH > 350 IU/L

53. At 48 hours:
 serum calcium < 8.0 mg/dL)
 Hematocrit fall >10%
 ARTERIAL PO2 < 60 mmHg)
 BUN RISE BY 5 or more mg/dL
 Base deficit (negative base excess) > 4 mEq/L
 Sequestration of fluids > 6 L

54. MORTALITY PREDICTION :
SCORE % MORTALITY
0-2 1%
3-4 16%
5-6 40%
7-8 100%

55. APACHE SCORE
"Acute Physiology And Chronic Health Evaluation" (APACHE
II) score > 8 points predicts 11% to 18% mortality
 Hemorrhagic peritoneal fluid
 Obesity
 Indicators of organ failure
 Hypotension (SBP <90 mmHG) or
 tachycardia > 130 beat/min
 PO2 <60 mmHg
 Oliguria (<50 mL/h) or increasing BUN and creatinine
 Serum calcium < 1.90 mmol/L (<8.0 mg/dL)
 serum albumin <33 g/L (<3.2.g/dL)

56. GLASGOW CRITERIA
 The Glasgow criteria is valid for both gallstone and alcohol induced
pancreatitis, whereas the Ranson score is only for alcohol induced
pancreatitis. If a patient scores 3 or more it indicates severe
pancreatitis and the patient should be transferred to ITU. It is scored
through the mnemonic, PANCREAS:
 P - PaO2 <8kPa
 A - Age >55 year old
 N - Neutrophilia -WCC >15x10(9)/L
 C - Calcium <2 mmol/L
 R - Renal function, Urea >16 mmol/L
 E - Enzymes: LDH >600iu/L; AST >200iu/L
 A - Albumin <32g/L (serum)
 S - Sugar: blood glucose >10 mmol/L

57. TREATMENT OF MILD DISEASE
 NPO
 PAIN CONTROL BY MEPRIDINE 100-150MG
I/M EVERY 4 HRS
 RESUME ORAL FLUIDS ONLY WHEN PAIN IS
SETTLED,BOWEL SOUNDS ARE AUDIBLE.
 CLEAR LIQUIDS ARE GIVEN FIRST
 SHIFT TO FAT FREE DIET LATER

58. TREATMENT OF SEVERE DISEASE:
 500-1000ML FOR SEVERAL HRS THEN 250-3—
ML TO MAIINTAIN INTRAVASCULAR VOLUME.
 MONITOR CA LEVELS AND REPLACE
ACCORDINGLY
 ALBUMIN OR FFP INFUSIONS FOR PATIENT
WITH COAGULOPATHY OR
HYPOALBUMINEMIA
 MONIOTR ABGS N CVP FOR FLUID
REPLACEMENT
 ANTIBIOTIC PROPHYLAXIS

59. FLUID REPLACEMENT
 Aggressive hydration at a rate of 5 to 10 mL/kg
per hour of isotonic crystalloid solution (eg,
normal saline or lactated Ringer’s solution) to all
patients with acute pancreatitis, unless
cardiovascular, renal, or other related comorbid
factors preclude aggressive fluid replacement.
 In patients with severe volume depletion that
manifests as hypotension and tachycardia, more
rapid repletion with 20 mL/kg of intravenous
fluid given over 30 minutes followed by 3
mL/kg/hour for 8 to 12 hours.[30][31]

60.  Fluid requirements should be reassessed at
frequent intervals in the first six hours of
admission and for the next 24 to 48 hours. The
rate of fluid resuscitation should be adjusted
based on clinical assessment, hematocrit and
blood urea nitrogen (BUN) values.
 35]
 There is some evidence that fluid resuscitation
with lactated Ringer’s solution may reduce the
incidence of Systemic Inflammatory Response
Syndrome (SIRS) as compared with normal
saline.[36]

61. PAIN CONTROL
 Meperidine, has been favored over morphine
for analgesia in pancreatitis because studies
showed that morphine caused an increase in
sphincter of Oddi pressure

62. BOWEL REST
In the management of acute pancreatitis, the
treatment is to stop feeding the patient, giving
him or her nothing by mouth, giving intravenous
fluids to prevent dehydration, and sufficient pain
control. As the pancreas is stimulated to secrete
enzymes by the presence of food in the stomach,
having no food pass through the system allows
the pancreas to rest.
Approximately 75% of relapses occur within 48
hours of oral refeeding.

63. NUTRITIONAL SUPPORT
 Recently, there has been a shift in the management paradigm from TPN
(total parenteral nutrition) to early, post-pyloric enteral feeding (in
which a feeding tube is endoscopically or radiographically introduced to
the third portion of the duodenum). The advantage of enteral feeding is
that it is more physiological, prevents gut mucosal atrophy, and is free
from the side effects of TPN (such as fungemia).
 Disadvantages of a naso-enteric feeding tube include increased risk of
sinusitis (especially if the tube remains in place greater than two weeks)
and a still-present risk of accidentally intubating the trachea even in
intubated patients (contrary to popular belief, the endotracheal tube
cuff alone is not always sufficient to prevent NG tube entry into the
trachea). Oxygen may be provided in some patients (about 30%) if Pao2
levels fall below 70mm of Hg.

64. ANTIBIOTICS(Carbapenems)
 IMIPENEM:
0.5 gram intravenously every eight hours for two
weeks showed a reduction in from pancreatic sepsis
from 30% to 12%.
 CEFUROXIME 1.5 G IV TDS FOR 14 DAYS REDUCES
THE RISK OF PANCREATIC INFECTION
MEROPENEM:
 A subsequent randomized controlled trial that used
meropenem 1 gram intravenously every 8 hours for 7
to 21 days stated no benefit

65. ERCP:
Early ERCP (endoscopic retrograde
cholangiopancreatography), performed
within 24 to 72 hours of presentation, is
known to reduce morbidity and mortality.[47]
The indications for early ERCP are as follows :
 Clinical deterioration or lack of improvement
after 24 hours
 Detection of common bile duct stones or
dilated intrahepatic or extrahepatic ducts on
CT abdomen

66.  The disadvantages of ERCP are as follows :
 ERCP precipitates pancreatitis, and can
introduce infection to sterile pancreatitis
 The inherent risks of ERCP i.e. bleeding
 It is worth noting that ERCP itself can be a
cause of pancreatitis.

67.  Surgery
 Surgery is indicated for
 (i) infected pancreatic necrosis
 (ii) diagnostic uncertainty
(iii) complications.

68. COMPLICATIONS
 Systemic complications
1. Metabolic
 Hypocalcemia, hyperglycemia, hypertriglyceridemia
 Respiratory
 Hypoxemia, atelectasis, Effusion, pneumonitis, Severe acute
respiratory syndrome (SARS) Renal
 Renal artery or vein thrombosis
 Renal failure
 Circulatory
 Arrhythmias
 Hypovolemia and shock
 myocardial infarct
 Pericardial effusion
 vascular thrombosis

69.  Gastrointestinal
 Gastrointestinal hemorrhage from stress
ulceration;
 gastric varices (secondary to splenic vein
thrombosis)
 Gastrointestinal obstruction
 Hepatobiliary
 Jaundice
 Portal vein thrombosis

70.  Neurologic
 Psychosis or encephalopathy (confusion, delusion and
coma)
 Cerebral Embolism
 Blindness (angiopathic retinopathy with hemorrhage)
 Hematologic
 Anemia
 DIC
 Leucocytosis
 Dermatologic
 Painful subcutaneous fat necrosis

71. FEATURES OF ACUTE VIRAL
HEPATITIS

72. FEATURES OF LEPTOSPIROSIS

73. MCQ 1
 WHICH OF THE FOLLOWING IS NOT A
CRITERIA IN RANSON SCORING OF ACUTE
PANCREATITIS?
 S/LDH
 S/CA
 S/LIPASE
 HCO3 LEVEL
 TLC COUNT

74. MCQ 2
 WHICH OF THE FOLLOWING IS THE GOLD
STANDARD INVESTIGATION FOR
DIAGNOSING SEVERE/NECROTIC
PANCREATITIS?
 USG ABDOMEN
 XRAY ABDOMEN
 TRIPLE PHASE CT ABDOMEN
 PET SCAN
 CATSCAN

75. MCQ 3:
 FOLLOWING IS THE MOST SPECIFIC
INDICATOR OF PANCREATIC INJURY?
 S/LDH
 S/TRIGLYCERIDE
 S/LIPASE
 S/AMYLASE
 HCT