case pancretitis

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?