Present illness 10 ชัวE โมงก่อนมาโรงพยาบาล มีอาการปวดทัวE ท้อง ปวดมากสุ ดบริ เวณสะดื อและลิD นปีE อาการเป็ นๆหายๆ มีช่วง ทีEหายสนิ ท ไม่ร้าวไปบริ เวณอืE น มีคลืE นไส้ อาเจียน 3-4 ครัDง อ่อนเพลี ย เวียนศีรษะ ไม่มีปัสสาวะแสบขัด ไม่มีถ่ายเหลว ไม่มีไข้ ไปตรวจทีEอนามัย มาแล้วแพทย์ให้ยาแก้ปวดท้อง ยา ลดกรดมาทาน อาการยังไม่ดีขD ึ น จึงมาโรงพยาบาล History Past medical history ◦ Underlying disease: DM on Glipizide (5) 1*1 po ac, Metformin 1*3 po pc DLP on Gemfibrozil (600) 2*1 po pc loss F/U 5 months ◦ S/P C/S 2561 , LC 29/1/2563
Personal history ◦ ปฏิเสธประวัติสูบบุหรีE ◦ ปฏิเสธประวัติดืEมแอลกอฮอล์/ใช้สารเสพติด
Family history ◦ มีประวัติคนในครอบครัวเป็ นโรคไขมันในเลือดสู ง Physical Examination ◦ Vital sign: T 37.7 c, pulse 118/min, RR 22/min, BP 115/90 mmHg ◦ General appearance: Good consciousness ◦ HEENT: No pale conjunctiva, anicteric sclera, no arcus cornealis ◦ CVS: Normal S1S2, no murmur ◦ RS: Equal breath sound , no adventitious sound ◦ ABD: Generalized mild tenderness, moderate tenderness at epigastric area, no rebound tenderness, no guarding ◦ EXT: No pitting edema ◦ Skin: No eruptive xanthoma, no tendon xanthema PROBLEM LIST ◦Acute epigastric pain with nausea and vomiting ◦Underlying DM, HT loss F/U Differential diagnosis Lab investigation? CBC WBC 16,130 cell/cumm Platelet count 325,000 cell/cumm RBC 4.58 x 106 cells Neutrophil 87.7 % HB 13.8 g/dl Lymphocyte 5.4 % Hct 37.0 % Monocyte 6.7 % MCV 80.9 fl Platelet smear Adequate MCHC 30.2 g/dl RBC morphology RDW 13.2 % Normochromia,normocytosis Urinary analysis Appearance clear WBC 0-1 cell/HPF color pale yellow RBC negative pH 5.0 Squamous epithelial cell 0-1 cell/HPF Sp.gr 1.032 Bacteria negative Protein 2+ Glucose 3+ Nitrite negative Ketone 2+ Urobilinogen normal Bilirubin negative Leukocyte negative Blood negative BUN 8.0 mg/dL Cr 0.32 mg/dL Sodium 123.4 mmol/L Potassium 3.8 mmol/L Chloride 90.0 mmol/L TCO2 13.0 mmol/L Calcium 7.5 mg/dL Magnesium 1.2 mEq/L Phosphorus 1.1 mg/dL Liver function test Total 10.1 g/dL Albumin 3.3 g/dL Globulin 6.8 g/dL Total bilirubin 0.3 mg/dL Direct bilirubin < 0.10 mg/dL Alkaline phosphatase 40 U/L Amylase 116 U/L Ketones 2.6 mmol/L Glucose 234.0 mg/dL Lactate 3.4 mmol/L Lipid profile Cholesterol 734 mg/dL Triglyceride 5612 mg/dL HDL 17 mg/dL LDL 21 mg/dL CT whole abdomen - Edematous change with heterogenousparenchymal enhancement of the pancreas, more at pancreatic head, with surrounding fat reticulation and low attenuation fluid at the peripancreatic, along transverse mesocolon, right anterior pararenal, right perinephric regions, right paracolic gutter and pelvic cavity. Suggestive of interstitial edematous pancreatitis, please correlate with clinical and laboratory findings. - Thickening wall of the ascending and transverse colon, probably infection/inflammation process. - Plate atelectasis in posterior basal segments of both lower lobes. DIAGNOSIS ◦Acute pancreatitis suspected from hypertriglyceridemia ◦Hyponatremia ◦Metabolic acidosis ◦Lactic acidosis ◦Hypocalcemia, hypomagnesemia, hypophosphatemia Management Acute pancreatitis suspected from hypertriglyceridemia
◦ NSS IV hydration ◦ Ceftriaxone 2 gm iv OD 27/9/64 - 4/10/64 (total 7 days) ◦ Metronidazole 500 mg IV q 8 hr 28/9/64 - 5/10/64 (total 7 days)
◦ H/CxII - NG 27/9/64 Management Hyponatremia: suspected from hypovolemia, hypertriglyceria Metabolic acidosis Lactic acidosis ◦ 0.9% NaCl 1500 ml IV load then continue hydration ◦ 3% NaCl 150 ml IV load in 20 min Management Hypocalcemia, hypophosphatemia, hypomagnesemia
- Glycophose 20 mmol + 0.9% NaCl 100 ml in 6 hr (total 4 doses)
- 50%MgSO4 IV drip (27-29/9/64), (1-3/10/64) - Continue MgO 1*2 po pc Acute pancreatitis Pathophysiology Diagnosis 1. Typical pancreatic-type pain 2. Rising serum lipase or amylase > 3-5 times of UNL Too early or too late, hyperTG, acute attack on top CP. Intestinal obstruction/ ischemia, renal insufficiency, acidosis. 3. Contrast-enhanced CT - A normal-looking pancreas does not exclude mild/early AP. - Not a prerequisite. Only when symptom and lab are discordant - DDx surgical condition e.g. perforation. Bedside Index for Severity of Acute Pancreatitis (BISAP) • BUN > 25 mg/dL • Impaired Mental Status • SIRS • Age > 60 • Pleural effusion
0 1 2 3 4 5 Mild Severe NPV ~ 90% PPV ~ 40% ICU:when? • Predicted to be severe • Already presence of organ failure • Elderly, co-morbidities of cardiac and renal disease Treatment Optimal early treatments to adjust the correct angle to hit the targets 1. Downgrade severity 2. Avoid complications 3. Reduce mortality Adequate hydration • Prevent pancreatic necrosis. Decrease mortality. • Isotonic crystalloid (NSS or RLS) 250-500 ml/hr, given within the first 12-24 hr, rapid loading if shock. • Use of goal-directed therapy for fluid management. • Reevaluate volume status every 4-6 hr in the first 48 hr. o Target: urine output, decrease in Hct, BUN and Cr, or CVP measurement. Early enteral nutrition within 24 hr. • Decrease LOS, infectious, morbidity. • Mild: oral low fat soft diet after improvement of nausea and abdominal pain. • Severe: enteral tube feeding, NG = NJ, avoid parenteral nutrition as increase infectious complications, safety concern of NG feeding - risk of aspiration. Antibiotics for extrapancreaticinfection • In patients with predicted severe AP and necrotizing pancreatitis, suggest against the use of prophylactic antibiotic. • Challenging diagnosis: inflammatory status vs. infectious complications. o Serum procalcitonin (PCT). Early phase: the first 7 days. • Causes of death: SIRS and multiorgan failure • Mild = recovery in early phase • C-reactive protein at 48 hours after symptoms onset > 150 mg/l = predictor of necrotizing pancreatitis Late phase: weeks to months •After 7-10 days and not recovery yet. •Presence of organ(s) failure, Local complication(s). •Cause of death = local complication(s) and infection. o Compensatory, anti-inflammatory response syndrome: increase rate of infection. Treatment of Complications (3D) • Sterile: no drainage. • Infected: clinical or imaging (air bubbles) • Delayed: least 4-12 wks with ATB = less mortality, less inflammation, max. liquefaction, strong wall-off necrosis or even no need for intervention. • Drainage: endoscopic > percutaneous. • Debride: endoscopic, video-assisted retroperitoneal, laparoscopic, open Sx. Hypertriglyceridemia Classification Etiology Management THANK YOU
24TH GAWAD KALASAG SEAL AND SPECIAL AWARDS FOR EXCELLENCE IN DISASTER RISK REDUCTION AND MANAGEMENT AND HUMANITARIAN ASSISTANCE CY 23024 OFFICIAL LIST OF WINNERS
24TH GAWAD KALASAG SEAL AND SPECIAL AWARDS FOR EXCELLENCE IN DISASTER RISK REDUCTION AND MANAGEMENT AND HUMANITARIAN ASSISTANCE CY 23024 OFFICIAL LIST OF WINNERS
