case pancretitis
TRANSCRIPT
بسم ال الرحمن الرحيم وزارة الدفاع
رئاسة الركان المشتركة الادارة العامة للخدمات الطبية
قسم العناية المكثفة
Presented by : Monalisa Al Binjawi Supervised by: 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 history and presentation
Peptic ulcer Gastritis Cholecystitis Acute pancreatitis Pneumonia Gastroenteritis Myocardial infarction
ill,tachypnic, not pale, jaundiced or cyanosed. vitals
pulse Blood pressure Respiratory rate temperature
86 110/60 20 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: 95 mg/l significant ≥ 10
RGB: 387
Renal profile:
Liver function tests
B. urea S. creatinin S. Na S.K S.Ca
31 mg/dl 1 g/dl 142 mmol/l 3.3 mmol/l 8.5mmol/l
Total bilirubin
Direct bilirubin
Total protein
S. Albumin
S. globulin
ALP AST ALT
0.3 mg/dl
0.2 mg/dl
6.9 g/dl
3.9 g/dl
3g/dl
37U/L
3.9U/L
39U/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.
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
©2012 UpToDate®
Etiology of acute pancreatitis
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 enzymesSerum 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
Antibiotics was upgraded to meropenem 1g bd inj
Non re-breathing mask 15l/min Non re-breathing mask 15l/min
Received about 3 liters of IV. Fluids (Normal saline)
Received about 3 liters of IV. Fluids (Normal saline)
Patient was admitted to the ICU Patient was admitted to the ICU
Insulin infusionInsulin infusion
Inotropes were started by portocol (noradrenaline, adrenaline)
Inotropes were started by portocol (noradrenaline, adrenaline)
Tachycardic. confused. Drowsy. Fatigue Anuric
ABG:
Renal profile:
bleeding profile
pH PCO2 PO2 HCO3 BEecf
7.09 40.5 80 12.4 -17.5
B. urea S. creatinin S. Na S.K S.Ca
76mg/dl 2.4 mg/dl 140mmol/l 5.6 mmol/l 8.8mmol/l
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)
it indicates that the tissue are extracting higher percentage of oxygen from the blood
than normal
pH PCO2 PO2 so2
6.9 65.6 10 40%
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?