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R4 王建中 /VS 吳允升 Apr, 11 st , 2014

R4 王建中 /VS 吳允升 Apr, 11 st , 2014. Critical Combine Conference. A 49-year-old man with left upper abdominal pain for about 3 months. Patient Profile. Systemic disease:

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R4 王建中 /VS 吳允升 Apr, 11 st , 2014

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  1. R4 王建中/VS 吳允升Apr, 11st, 2014 Critical Combine Conference

  2. A49-year-old man with left upper abdominal pain for about 3 months

  3. Patient Profile • Systemic disease: • Gastric adenocarcinoma, cT4bNxM1, inoperable and metastatic, pancreas invasion and peritoneal seedings/carcnomatosis with ileus, stage IV • Obstructive uropathy with hydronephrosis due to cancer • Operation: • 2014/02/17: Port-A implantation, echo-guided • Allergy: NKA • Personal history: • Smoking & alcohol use: Nil • Education:Junior high school • Marital status: Married

  4. Patient Profile • Occupation:服務業 • Drug history: • Nexium (40) 1 tab QD • Strocain 1 tab TID • Gascon (40) 1 tab TID

  5. Family History No HTN, CAD, Autoimmune Disease HX 77 y/o 49 y/o 49 y/o 20 y/o 19 y/o

  6. Past History 2013 • Left upper abdominal sharp pain • Not correlated to oral intake • Easy satiety and abdominal distention •  Visit 新泰 hospital: EGD : gastric ulce Dec • Persistent abdominal pain • Weight loss about 9kgs in one months • Bowel habit change was noted. •  新光 H: • EGD : one large ulcer about 1.5~2cm with elevated • margin and folds convergence in the angle to the • LC/posterior wall of lower body, suspected • malignancy •  Biopsy performed • CT scan : gastric cancer with peritoneal seeding 2014 Jan, 21

  7. Past History 2014 • Laparoscopic appentectomy was done for suspicious of acute appendicitis • Peritoneal seeding was noted during surgical intervention  Pathology: metastatic adenocarcinoma Jan, 21 Jan, 21 NTUH • MRI : infiltrative tumor with involvement of stomach and pancreas, probably arising from gastric cancer and directly invading the pancreas; multiple regional lymph nodes Feb, 12

  8. Abdominal MRI (2014.02.12) Infiltrative gastric tumor with involvement of stomach and pancreas; multiple regional lymph nodes

  9. Physical Examination BH: 170cm BW:68.7Kg BMI:23.77 HEENT Conjunctiva: not pale, Sclera: icteric (-) Pupil: isocoric, 4mm/4mm, midposition Light reflex: R/L +/+, promptly Oral thrush(-), oral ulcers(-) Neck Supple, tightness(-), JVE(-) , LAP(-), goiter(-) Kernig’s sign (-), Brudzinski’s sign(-)

  10. Chest Symmetrically expanded, axillary LAP(-) Breath sound: clear over bilateral lower lung fields Heart PMI displacement (-),RHB, thrill(-) Murmur(-), distant heart sound (-) Abdomen Distended, normoactive bowel sound, Tenderness(+, epigastric area) Hepatosplenomegaly (-), Extremity Petechiae(-), purpura(-), cyanosis(-), cold (-) Leg edema(-), clubbing finger(-) Physical Examination

  11. CXR 201402/17

  12. ECG (2014.02.14)

  13. Past History 2014 • Port-Ainsertion • Initiate TPN Feb, 17 • EGD:Advanced gastric cancer, Bormann type 3, angle to the LC-PW of lower body, s/p biopsy • Pathology: adenocarcinoma, poorly-differentiated Feb, 19 • Double J (Tumor stent) insertion • for left hydronephrosis Feb, 22

  14. Past History 2014 • HDFL C1D1 • NG decompensation: more than 2000ml gastric juice drained out per day • Keep TPN and keep I/O balance Feb, 25

  15. Laboratory Data 2/27: Cl:93 mmol/L

  16. Urine exam 2014/02/24 FENa =1.8% > 1%

  17. Renal Echography (2014.02.27) • Right • Size : normal 13.6 cm • Shape : regular • Cortical echogenecity : • increased chogenecity • Cortical thickness : • Normal: 2.0 cm • Central echo : mildly • seperated • Cystic lesion(s): Nil • Solid lesion : Nil • Left • Size : normal 12.1 cm • Shape : regular • Cortical echogenecity : • increased echogenecity • Cortical thickness : • Normal: 1.8 cm • Central echo : mildly • seperated • Cystic lesion(s): Nil • Solid lesion : Nil IMPRESSION : 1. Bilateral parenchymal renal disease 2. Moderate right hydronephrosis 3. Renal cyst, right 4. Engorged right renal vessels, r/o renal vein thrombosis

  18. Acute kidney injury Hypovolemia Decreased cardiac output Decreased effective circulating volume: -Congestive heart failure -Liver failure Impaired renal autoregulation: NSAIDS, ACEI/ARB, cyclosporin Prerenal Gluomerular: acute glomerulonephritis Intrinsic Tubules and interstitium Vascular: vasculitis, malignant hypertension, TTP-HUS Bladder outlet obstruction Bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidney) Postrenal Harrison's Principles of Internal Medicine, 18e

  19. Past History 2014 • Increased O2 demand suddenly • NG decompression: about 2600-3300ml/day • Suspected septic shock Mar, 04 Mar, 05 Mar, 05 Mar, 05 • Consult nephrologist; transfer to MICU? • DNR(+) • Family decided to discontinue inotropic agents • Passed away Mar, 06

  20. Final Diagnosis • Gastric adenocarcinoma, cT4bNxM1, stage IV, inoperable and metastatic, pancreas invasion and peritoneal seedings/carcnomatosis with ileus • Severe metabolic alkalosis secondary to hydrogen ion loss from vomiting (obstructive GI tract) • Acute kidney injury, AKIN stage 3 • Septic shock, suspected IAI related • Obstructive uropathy with hydronephrosis due to cancer

  21. Discussion-- Metabolic alkalosis The rule of dialysis for treatment for severe metabolic alkalosis

  22. Metabolic alkalosis

  23. F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  24. F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  25. F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  26. HSD11B2 gene KCNJ1 gene SCNN1B gene F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  27. Metabolic alkalosis • (1) Abnormal chloride losses • (2) In states of mineralocorticoid excess • (3) Renal ion transport disrupted by genetic abnormalities that lead to stimulation of collecting duct sodium reabsorption through ENaC (eg, Liddle syndrome) F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  28. Metabolic alkalosis • Surreptitious vomiting or diuretic abuse should always be considered • Both aldosterone and renin levels should be increased • Apparent mineralocorticoid syndrome • Liddle syndrome • HSD2 deficiency • Hypertension • Hypokalemia • Metabolic alkalosis • Low aldosterone levels • Genetic analysis: gold standard • Aldosterone antagonist: for 11HSD2 • deficiency; no effect to Liddle syndrome • Amiloride: blocks ENaC directly, • treatment for Liddle syndrome F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135

  29. Clinical course of a patient with CHF and metabolic alkalosis

  30. Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  31. Case Present • 68 y/o M, transferred to ICU: Af and pulmonary edema s/p intubation • HTN, CAD,CHF with preserved systolic function, obesity • Persistent signs of volume overload but received only intermittent doses of furosemide • Three days prior to transfer, developed more overt signs of CHF, prompting more aggressive use of furosemide (40-80 mg intravenously [IV] twice daily) Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  32. Case Present • Remained volume overloaded and developed pulmonary edema requiring intubation during an episode of rapid Afib • Echocardiogram: atrial dilatation, moderate AR and MR, LVEF: 50% with mild posterobasal hypokinesis, and impaired diastolic filling • IV furosemide with gradual improvement in congestion  progressive alkalemia and severe hypokalemia over the ensuing 5 days Diagnosis: CHF; metabolic alkalosis due to heart failure and loop diuretic use; hypokalemia due to loop diuretic use and secondary hyperaldosteronism from decompensated heart failure Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  33. Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  34. Metabolic alkalosis of CHF • Diuretic therapy: chloride loss, decreased effective circulating volume, activation of the renin-angiotensin-aldosterone system • CHF: system sympathetic overactivity  increased renal adrenergic tone  activation of the sodium/hydrogen ion exchanger in the proximal tubule Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  35. Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  36. IV acetazolamide (250 mg every 6 hours for 24 hours or as a single dose of 500 mg) Ex: 70 kg*0.5*10 mEq; infusion should not be faster than 0.2 mEq of hydrogen per 1 kg of body weight per hour; F/U e-/ABG Q1-2H Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827

  37. The rule of dialysis for treatment for severe metabolic alkalosis

  38. Case Present • A 69-year-old woman, ESRD (secondary to hypertensive nephrosclerosis); invasive SCC of the left pinna and ear with neck metastasis • Presented with confusion, lethargy, and low oxygen saturation (80%) • These symptoms preceded for several days of severe and profuse vomiting • Abdominal CT: proximal small-bowel dilatation measuring up to 3.3 cm in diameter, with a transition point noted in the left hemipelvis (narcotic use) Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  39. Case Present • Admitted to ICU: • NG insertion, pantoprazole therapy • Dialysis: urgently for 3 hours without ultrafiltration: using dialysate: • Potassium : 4 mEq/L (4 mmol/L) • Calcium(ionized): 5 mg/dL (1.25 mmol/L) • Bicarbonate: 30 mEq/L (30 mmol/L) Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  40. NG 4700ml iHD iHD 2hours Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  41. Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  42. + Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  43. Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  44. Vomiting and GI hydrogen ion loss • High grade gastric distension due to outlet obstruction causes cholinergic activation  Increased gastrin secretion, decreased somatostatin secretion  Increased hydrogen ion secretion and gastric fluid volume • When stimulated, gastric fluid has a hydrogen ion concentration of 100-170 mmol/L (pH 1.0) • No stimulated: hydrogen ion concentration 10 mmol/L • One millimole of bicarbonate is generated in body fluids for each millimole of hydrogen ion lost in emesis Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  45. Hemodialysis for severe metabolic alkalosis • Severe metabolic alkalosis (serum bicarbonate concentrations > 50 mEq/L): • Hemodialysis with a reduced bath bicarbonate concentration is a safe and effective intervention • Bicarbonate decreased to the lowest level available • No increase calcium concentration • Hydrochloric acid infusion is not an acceptable treatment alternative in patients without kidney function (large volume of fluid) Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  46. Lu Huber, Am J Kidney Dis. 2011;58(1):144-149

  47. Take Home Message • Severe metabolic alkalosis (bicarbonate cncentration >50 mEq/L) + (all these severe case reports) with impairment of kidney function (due to volume loss) Hemodialysis may be considered ! • For metabolic alkalosis, treatment the underlying disease is most important

  48. Thank you for your attention!

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