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‫بسم ال الرحمن الرحيم‬
‫وزارة الدفاع‬
‫رئاسة الركان المشتركة‬
‫الادارة العامة للخدمات الطبية‬
‫قسم العناية المكثفة‬
Presented by :
Supervised by:

Monalisa Al Binjawi
Dr. kamal O. Mergani
A 55 years old Diabetic female presented
to the ER on the 22 of October complaining
of:
•
•

Epigastric pain
Vomiting

12 hours
No significant past medical or surgical
history.
 She has a family history of diabetes
 Drug history :
- Oral hypoglycemic agents .. Glimepride
off treatment for 2 months

Based

on his
tory a
nd

prese
ntatio
n
 Peptic ulcer
 Gastritis
 Cholecystitis
 Acute pancreatitis
 Pneumonia
 Gastroenteritis
 Myocardial infarction
 ill,tachypnic, not pale, jaundiced or cyanosed.
 vitals

pulse
86

Blood pressure Respiratory rate
110/60

20

temperature
febrile
 CNS: Confused, GCS: 14/15
 CVS: Normal heart sounds, no murmers.


Respiratory: Good air flow, no added sound
on auscultation.

 Abdominal tenderness at epigastric area, no

palpable masses.


CBC :

 C. reactive protein:
 RGB:

387

95 mg/l

significant ≥ 10
 Renal profile:
B. urea

S. creatinin

31 mg/dl

1 g/dl

S. Na

S.K

142 mmol/l

3.3 mmol/l

S.Ca
8.5mmol/l

 Liver function tests
Total
Direct
bilirubin bilirubin
0.3
mg/dl

0.2
mg/dl

Total
protein

S.
Albumin

S.
globulin

ALP

AST

ALT

6.9
g/dl

3.9
g/dl

3
g/dl

37
U/L

3.9
U/L

39
U/L
 Bleeding profile
PT

PTT

INR

28.1

34

1.4
 Pancreas:

edematous, hypo echoic, with
calcifications.

 liver, gall bladder, spleen, kidneys, urinary

bladder were normal with no marked
significance.

 No ascitis.
 Serum amylase: 1500
 ABG:
pH

PCO2

PO2

HCO3

BEecf

7.250

23.2

71

10.2

-15.2
 Sepsis

Metabolic acidosis
 High pancreatic enzyme

 NPO.
 IV. FLUIDS 125 ml/ hr.
 Antibiotics ( ceftrixon , metronidazol).
 PPI.
 KCl 20 mmol in N.S over 4 hours.
 RBG 4 hourly and soluable insulin with sliding

scale accordingly s/c.
 Enoxaparine( Clexane®) 40 mg.
 Planed for an abdominal CT.
 Acute pancreatitis is an inflammatory condition

of the pancreas characterized clinically by
abdominal pain and elevated levels of
pancreatic enzymes in the blood.
 The pathogenesis of acute pancreatitis is not

fully understood. Nevertheless, a number of
conditions are known to induce this disorder
with varying degrees of certainty, with
gallstones and chronic alcohol abuse
accounting for majority of cases.
©2012 UpToDate®

Etiology of acute pancreatitis
Mechanical

Gallstones, biliary sludge, ascariasis, periampullary diverticulum, pancreatic or periampullary cancer,
ampullary stenosis, duodenal stricture or obstruction

Toxic

Ethanol, methanol, scorpion venom, organophosphate poisoning

Metabolic

Hyperlipidemia (types I, IV, V), hypercalcemia

Drugs

Didanosine, pentamidine, metronidazole, stibogluconate, tetracycline furosemide, thiazides,
sulphasalazine, 5-ASA, L-asparaginase, azathioprine, valproic acid, sulindac, salicylates, calcium,
estrogen

Infection

Viruses-mumps, coxsackie, hepatitis B, CMV, varicella-zoster, HSV, HIV
Bacteria-mycoplasma, Legionella, Leptospira, salmonella
Fungi-aspergillus
Parasites-toxoplasma, cryptosporidium, Ascaris

Trauma

Blunt or penetrating abdominal injury, iatrogenic injury during surgery or ERCP (sphincterotomy)

Congenital

Cholodochocele type V, ? pancreas divisum

Vascular

Ischemia, atheroembolism, vasculitis (polyarteritis nodosa, SLE)

Miscellaneous

Post ERCP, pregnancy, renal transplantation, alpha-1-antitrypsin deficiency

Genetic

CFTR and other genetic mutations
 Acute pancreatitis can be suspected clinically,

but requires biochemical, radiologic, and
sometimes histologic evidence to confirm the
diagnosis.
 none of them alone is diagnostic.
 Abdominal pain at epigastric area or

radiating to the back.
It worsen after eating.
 Nausea.
 Vomiting.
 Tender abdomen.
 Indigestion.
 Oily smelly stool.
 Pancreatic enzymes

Serum lipase and serum amylase.
Currently guidelines suggest that lipase
measurement is the most sensitive marker
for diagnosis of acute pancreatitis.
 A commonly used classification system (the

Atlanta classification) divides AP into two
broad categories:
Mild (edematous and interstitial) acute
pancreatitis.
Severe (usually synonymous with necrotizing)
acute pancreatitis.
 The criteria for severe AP included any of the

following:
 A Ranson's score of 3 or more
 An APACHE II score of 8 or more within the
first 48 hours
 Organ failure (respiratory, circulatory, renal,
and/or gastrointestinal bleeding)
 Local complications (pancreatic necrosis,
abscess, or pseudocyst).
 When do you do “early” transfer to ICU?
 When do you consult critical care team?
 When do you start antibiotics?
 “They” say people crash fast – who are these

people?
 What is “aggressive fluid resuscitation?”
 Early identification of severity and

appropriate ICU care has significantly
reduced mortality over the last 20 years.
0 hours
Age

>55

White blood cell count

>16,000/mm3

Blood glucose

>200 mg/dL (11.1 mmol/L)

Lactate dehydrogenase

>350 U/L

Aspartate aminotransferase
(AST)

>250 U/L

48 hours
Hematocrit

Fall by ≥10 percent

Blood urea nitrogen

Increase by ≥5 mg/dL (1.8 mmol/L) despite
fluids

Serum calcium

<8 mg/dL (2 mmol/L)

pO2

<60 mmHg

Base deficit

>4 MEq/L

Fluid sequestation

>6000 mL
 <2 signs ……… With 5% risk of mortality
 3-4 signs …….. With 15-20% risk of mortality
 5-6 signs …….. With 40%
 >7 signs …….. With 99% risk of mortality
 Scoring systems for ICU and surgical patients:
 APACHE II (Acute Physiology And Chronic

Health Evaluation)

≥ 8 is severe
 Patient became very ill, febrile, distress ,

tachycardic and desaturated with a
saturation of 92% and irrecordable blood
pressure and uncontrolled blood glucose
PATIENT WENT
INTO SEPTIC
SHOCK
Non re-breathing mask 15l/min
Non re-breathing mask 15l/min
Received about 33liters of IV. Fluids
Received about liters of IV. Fluids
(Normal saline)
(Normal saline)

Patient was admitted to the ICU
Patient was admitted to the ICU

Insulin infusion
Insulin infusion
Inotropes were started by portocol
Inotropes were started by portocol
(noradrenaline, adrenaline)
(noradrenaline, adrenaline)

Antibiotics was upgraded to
meropenem 1g bd inj
 Tachycardic.
 confused.
 Drowsy.
 Fatigue
 Anuric
 ABG:
pH

PCO2

PO2

HCO3

BEecf

7.09

40.5

80

12.4

-17.5

 Renal profile:
B. urea

S. creatinin

S. Na

76mg/dl

2.4 mg/dl

140mmol/l

S.K

S.Ca

5.6 mmol/l 8.8mmol/l

 bleeding profile
PT

PTT

INR

28.7

39.5

2.6
At this point
 Septic shock.
 Sever decomensated metabolic acidosis.
 Acute kidney injury (anuric)
 Prolonged bleeding profile
What is it?
 SvO2( mixed venous oxygen saturation)

It is the percentage of oxygen bounded to
hemoglobin in blood retaining to the right side of the
heart.
 It reflects the amount of oxygen “left over” after the
tissue extracts its need.
 Normal value > 70%

 SvO2( mixed venous oxygen saturation)
pH

PCO2

PO2

so2

6.9

65.6

10

40%

 it indicates that the tissue are extracting
 higher percentage of oxygen from the blood

than normal
 Shock
 ARDS
 DIC
 pseudocyst
Treatment of acute pancreatitis is based upon the
severity of the condition:


Mild AP
supportive care (pain control, IV
fluids, and correction of electrolyte and metabolic
abnormalities.



Severe AP
intensive care unit monitoring
and support of pulmonary, renal, circulatory, and
hepatobiliary function may minimize systemic
sequelae
 Adequate fluid.
 Adequate analgesia.
 antibiotics
 May require 250-500 cc/hr for first 48 hrs
▪ 6 L of fluid is sequestered in abdomen alone
▪ Third spacing can consume up to 1/3 of total plasma
volume
▪ Inadequate hydration can lead to hypotension and
acute tubular necrosis.
▪ aggressive fluid replacement can lead to peripheral and
pulmonary edema
 You may create electrolyte imbalances that need

to be corrected
 You may need CVP monitoring (central line)
 CXRs help (CHF vs ARDS)
 ABGs help (still hypoxic  need more fluids?)
 How do you know you are resuscitated?
 Blood pressure
 Heart rate
 Urine output
 SPO2/ABG’s show good oxygenation and no

acidemia
0.5 cc/kg/hr urine
output is goal
 Controversial
 They

Do decrease incidence of infection in
necrosis, but do NOT decrease mortality

 Imipenem
 Ciprofoxacine + metronidazole
 One study showed 24% of pts had fungus
 Pancreatic stimulation during AP releases

proteolytic enzymes  autodigestion
 Oral feeding increases release of secretin and
cholecystokinin  stim pancreas
 “rest the pancreas”  “NPO”
 In patients with severe acute pancreatitis
Enteral feeding is recommended rather than
parentral feeding
 In patients with severe acute pancreatitis

Enteral feeding is recommended rather than
parentral feeding.
▪ Easier to restart with
▪ Average length of nutritional support shorter
▪ 7 vs 11 days

▪ Fewer septic complications
▪ It cost much less
▪ Compared early vs delayed ENTERAL
feedings in 753 critically ill pts
▪ Early was 36 hrs!
Improved:
- Wound healing
- Host immune function
- Preservation of intestinal mucosal integrity
- Decreased infections
 Oxygenation:

- o2 supply ( So2> 94%)

-Liberal intubation/ventilation to treat ARDS



DVT prophylaxis.
 Patient became hypoxic.
 Blood pressure is still irrecordable.
 Further ABGs showed also sever

decompensated metabolic acidosis
 Patient went into cardiac arrest .
 Cardiopulmonary resuscitation was done but

patient didnt recover.
 Acute pancreatitis is a common illness

with many potential highly morbid
complications.
 Many cases are diagnose clinically and
managed supportively with bowel
rest, aggressive fluid administration
and analgesics.
 Early intensive care unit admission
decreases mortality.
ANY QUESTION?

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Case pancretitis

  • 1. ‫بسم ال الرحمن الرحيم‬ ‫وزارة الدفاع‬ ‫رئاسة الركان المشتركة‬ ‫الادارة العامة للخدمات الطبية‬ ‫قسم العناية المكثفة‬
  • 2.
  • 3. Presented by : Supervised by: Monalisa Al Binjawi Dr. kamal O. Mergani
  • 4. A 55 years old Diabetic female presented to the ER on the 22 of October complaining of:
  • 6. No significant past medical or surgical history.  She has a family history of diabetes  Drug history : - Oral hypoglycemic agents .. Glimepride off treatment for 2 months 
  • 8.  Peptic ulcer  Gastritis  Cholecystitis  Acute pancreatitis  Pneumonia  Gastroenteritis  Myocardial infarction
  • 9.  ill,tachypnic, not pale, jaundiced or cyanosed.  vitals pulse 86 Blood pressure Respiratory rate 110/60 20 temperature febrile
  • 10.  CNS: Confused, GCS: 14/15  CVS: Normal heart sounds, no murmers.  Respiratory: Good air flow, no added sound on auscultation.  Abdominal tenderness at epigastric area, no palpable masses.
  • 11.
  • 12.  CBC :  C. reactive protein:  RGB: 387 95 mg/l significant ≥ 10
  • 13.  Renal profile: B. urea S. creatinin 31 mg/dl 1 g/dl S. Na S.K 142 mmol/l 3.3 mmol/l S.Ca 8.5mmol/l  Liver function tests Total Direct bilirubin bilirubin 0.3 mg/dl 0.2 mg/dl Total protein S. Albumin S. globulin ALP AST ALT 6.9 g/dl 3.9 g/dl 3 g/dl 37 U/L 3.9 U/L 39 U/L
  • 15.
  • 16.
  • 17.
  • 18.
  • 19.  Pancreas: edematous, hypo echoic, with calcifications.  liver, gall bladder, spleen, kidneys, urinary bladder were normal with no marked significance.  No ascitis.
  • 20.  Serum amylase: 1500  ABG: pH PCO2 PO2 HCO3 BEecf 7.250 23.2 71 10.2 -15.2
  • 21.  Sepsis Metabolic acidosis  High pancreatic enzyme 
  • 22.
  • 23.  NPO.  IV. FLUIDS 125 ml/ hr.  Antibiotics ( ceftrixon , metronidazol).  PPI.  KCl 20 mmol in N.S over 4 hours.  RBG 4 hourly and soluable insulin with sliding scale accordingly s/c.  Enoxaparine( Clexane®) 40 mg.  Planed for an abdominal CT.
  • 24.  Acute pancreatitis is an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood.
  • 25.  The pathogenesis of acute pancreatitis is not fully understood. Nevertheless, a number of conditions are known to induce this disorder with varying degrees of certainty, with gallstones and chronic alcohol abuse accounting for majority of cases.
  • 26. ©2012 UpToDate® Etiology of acute pancreatitis Mechanical Gallstones, biliary sludge, ascariasis, periampullary diverticulum, pancreatic or periampullary cancer, ampullary stenosis, duodenal stricture or obstruction Toxic Ethanol, methanol, scorpion venom, organophosphate poisoning Metabolic Hyperlipidemia (types I, IV, V), hypercalcemia Drugs Didanosine, pentamidine, metronidazole, stibogluconate, tetracycline furosemide, thiazides, sulphasalazine, 5-ASA, L-asparaginase, azathioprine, valproic acid, sulindac, salicylates, calcium, estrogen Infection Viruses-mumps, coxsackie, hepatitis B, CMV, varicella-zoster, HSV, HIV Bacteria-mycoplasma, Legionella, Leptospira, salmonella Fungi-aspergillus Parasites-toxoplasma, cryptosporidium, Ascaris Trauma Blunt or penetrating abdominal injury, iatrogenic injury during surgery or ERCP (sphincterotomy) Congenital Cholodochocele type V, ? pancreas divisum Vascular Ischemia, atheroembolism, vasculitis (polyarteritis nodosa, SLE) Miscellaneous Post ERCP, pregnancy, renal transplantation, alpha-1-antitrypsin deficiency Genetic CFTR and other genetic mutations
  • 27.  Acute pancreatitis can be suspected clinically, but requires biochemical, radiologic, and sometimes histologic evidence to confirm the diagnosis.  none of them alone is diagnostic.
  • 28.  Abdominal pain at epigastric area or radiating to the back. It worsen after eating.  Nausea.  Vomiting.  Tender abdomen.  Indigestion.  Oily smelly stool.
  • 29.  Pancreatic enzymes Serum lipase and serum amylase. Currently guidelines suggest that lipase measurement is the most sensitive marker for diagnosis of acute pancreatitis.
  • 30.  A commonly used classification system (the Atlanta classification) divides AP into two broad categories: Mild (edematous and interstitial) acute pancreatitis. Severe (usually synonymous with necrotizing) acute pancreatitis.
  • 31.  The criteria for severe AP included any of the following:  A Ranson's score of 3 or more  An APACHE II score of 8 or more within the first 48 hours  Organ failure (respiratory, circulatory, renal, and/or gastrointestinal bleeding)  Local complications (pancreatic necrosis, abscess, or pseudocyst).
  • 32.  When do you do “early” transfer to ICU?  When do you consult critical care team?  When do you start antibiotics?  “They” say people crash fast – who are these people?  What is “aggressive fluid resuscitation?”
  • 33.  Early identification of severity and appropriate ICU care has significantly reduced mortality over the last 20 years.
  • 34. 0 hours Age >55 White blood cell count >16,000/mm3 Blood glucose >200 mg/dL (11.1 mmol/L) Lactate dehydrogenase >350 U/L Aspartate aminotransferase (AST) >250 U/L 48 hours Hematocrit Fall by ≥10 percent Blood urea nitrogen Increase by ≥5 mg/dL (1.8 mmol/L) despite fluids Serum calcium <8 mg/dL (2 mmol/L) pO2 <60 mmHg Base deficit >4 MEq/L Fluid sequestation >6000 mL
  • 35.  <2 signs ……… With 5% risk of mortality  3-4 signs …….. With 15-20% risk of mortality  5-6 signs …….. With 40%  >7 signs …….. With 99% risk of mortality
  • 36.  Scoring systems for ICU and surgical patients:  APACHE II (Acute Physiology And Chronic Health Evaluation) ≥ 8 is severe
  • 37.  Patient became very ill, febrile, distress , tachycardic and desaturated with a saturation of 92% and irrecordable blood pressure and uncontrolled blood glucose
  • 39. Non re-breathing mask 15l/min Non re-breathing mask 15l/min Received about 33liters of IV. Fluids Received about liters of IV. Fluids (Normal saline) (Normal saline) Patient was admitted to the ICU Patient was admitted to the ICU Insulin infusion Insulin infusion Inotropes were started by portocol Inotropes were started by portocol (noradrenaline, adrenaline) (noradrenaline, adrenaline) Antibiotics was upgraded to meropenem 1g bd inj
  • 40.  Tachycardic.  confused.  Drowsy.  Fatigue  Anuric
  • 41.  ABG: pH PCO2 PO2 HCO3 BEecf 7.09 40.5 80 12.4 -17.5  Renal profile: B. urea S. creatinin S. Na 76mg/dl 2.4 mg/dl 140mmol/l S.K S.Ca 5.6 mmol/l 8.8mmol/l  bleeding profile PT PTT INR 28.7 39.5 2.6
  • 43.  Septic shock.  Sever decomensated metabolic acidosis.  Acute kidney injury (anuric)  Prolonged bleeding profile
  • 44.
  • 46.  SvO2( mixed venous oxygen saturation) It is the percentage of oxygen bounded to hemoglobin in blood retaining to the right side of the heart.  It reflects the amount of oxygen “left over” after the tissue extracts its need.  Normal value > 70% 
  • 47.  SvO2( mixed venous oxygen saturation) pH PCO2 PO2 so2 6.9 65.6 10 40%  it indicates that the tissue are extracting  higher percentage of oxygen from the blood than normal
  • 48.  Shock  ARDS  DIC  pseudocyst
  • 49.
  • 50. Treatment of acute pancreatitis is based upon the severity of the condition:  Mild AP supportive care (pain control, IV fluids, and correction of electrolyte and metabolic abnormalities.  Severe AP intensive care unit monitoring and support of pulmonary, renal, circulatory, and hepatobiliary function may minimize systemic sequelae
  • 51.  Adequate fluid.  Adequate analgesia.  antibiotics
  • 52.  May require 250-500 cc/hr for first 48 hrs ▪ 6 L of fluid is sequestered in abdomen alone ▪ Third spacing can consume up to 1/3 of total plasma volume ▪ Inadequate hydration can lead to hypotension and acute tubular necrosis. ▪ aggressive fluid replacement can lead to peripheral and pulmonary edema
  • 53.
  • 54.  You may create electrolyte imbalances that need to be corrected  You may need CVP monitoring (central line)  CXRs help (CHF vs ARDS)  ABGs help (still hypoxic  need more fluids?)
  • 55.  How do you know you are resuscitated?  Blood pressure  Heart rate  Urine output  SPO2/ABG’s show good oxygenation and no acidemia
  • 57.  Controversial  They Do decrease incidence of infection in necrosis, but do NOT decrease mortality  Imipenem  Ciprofoxacine + metronidazole  One study showed 24% of pts had fungus
  • 58.  Pancreatic stimulation during AP releases proteolytic enzymes  autodigestion  Oral feeding increases release of secretin and cholecystokinin  stim pancreas  “rest the pancreas”  “NPO”  In patients with severe acute pancreatitis Enteral feeding is recommended rather than parentral feeding
  • 59.  In patients with severe acute pancreatitis Enteral feeding is recommended rather than parentral feeding. ▪ Easier to restart with ▪ Average length of nutritional support shorter ▪ 7 vs 11 days ▪ Fewer septic complications ▪ It cost much less
  • 60. ▪ Compared early vs delayed ENTERAL feedings in 753 critically ill pts ▪ Early was 36 hrs! Improved: - Wound healing - Host immune function - Preservation of intestinal mucosal integrity - Decreased infections
  • 61.  Oxygenation: - o2 supply ( So2> 94%) -Liberal intubation/ventilation to treat ARDS  DVT prophylaxis.
  • 62.  Patient became hypoxic.  Blood pressure is still irrecordable.  Further ABGs showed also sever decompensated metabolic acidosis
  • 63.
  • 64.  Patient went into cardiac arrest .  Cardiopulmonary resuscitation was done but patient didnt recover.
  • 65.  Acute pancreatitis is a common illness with many potential highly morbid complications.  Many cases are diagnose clinically and managed supportively with bowel rest, aggressive fluid administration and analgesics.  Early intensive care unit admission decreases mortality.

Editor's Notes

  1. Pain was constant sever not radiating to any area, notaggravated or relieved by any factor associated with vomiting of large amounts, not containing blood.
  2. Based on guidelines of sepsis management 2012
  3. Very poor prognosis
  4. 1- it usually takes 24-48 hrs
  5. $23/day vs $222/day