critical combine conference r4 王建中 /vs 吳允升 apr, 11 st, 2014
TRANSCRIPT
Critical Combine Conference
R4 王建中 /VS 吳允升Apr, 11st, 2014
A 49-year-old man with left upper abdominal
pain for about 3 months
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
Patient Profile
Occupation:服務業 Drug history:
Nexium (40) 1 tab QD Strocain 1 tab TID Gascon (40) 1 tab TID
Family History
49 y/o
No HTN, CAD, Autoimmune Disease HX
49 y/o
20 y/o 19 y/o
77 y/o
Past History2013
Jan, 21
Dec
Left upper abdominal sharp pain Not correlated to oral intake Easy satiety and abdominal distention Visit 新泰 hospital: EGD : gastric ulce
2014 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
Past History2014
Jan, 21
Laparoscopic appentectomy was done for suspicious of acute appendicitis Peritoneal seeding was noted during surgical intervention Pathology: metastatic adenocarcinoma
Jan, 21
Feb, 12
NTUH MRI : infiltrative tumor with involvement of stomach and pancreas, probably arising from gastric cancer and directly invading the pancreas; multiple regional lymph nodes
Abdominal MRI (2014.02.12)
Infiltrative gastric tumor with involvement of stomach and pancreas; multiple regional lymph nodes
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(-)
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
CXR 201402/17
ECG (2014.02.14)
Past History2014
Port-A insertion 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 hydronephrosisFeb, 22
Past History2014
HDFL C1D1 NG decompensation: more than 2000ml gastric juice drained out per day Keep TPN and keep I/O balance
Feb, 25
Laboratory Data
2/27: Cl:93 mmol/L
Sp.Gr. PH Protein Glu Ketone OB Bil Uro bil
mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL
1.031 6.0 100 (2+) - - 3+ - <1.5
RBC WBC Epith. Cast Crystal Nit. color
(/HPF) (/HPF) (/HPF) (/LPF)
>100 20-35 0-2 Granular cast - - cloudy, yellow
Urine exam 2014/02/24
Cre Na
mg/dL mmole/L
62 68
FENa =1.8% > 1%FENa =1.8% > 1%
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
IMPRESSION : 1. Bilateral parenchymal renal disease 2. Moderate right hydronephrosis 3. Renal cyst, right 4. Engorged right renal vessels, r/o renal vein thrombosis
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
Acute kidney injury
Prerenal
Intrinsic
Postrenal
Hypovolemia Decreased cardiac output
Decreased effective circulating volume: -Congestive heart failure
-Liver failure Impaired renal autoregulation: NSAIDS, ACEI/ARB, cyclosporin
Gluomerular: acute glomerulonephritis
Tubules and interstitium
Vascular: vasculitis, malignant hypertension, TTP-HUS
Bladder outlet obstruction Bilateral pelvoureteral obstruction
(or unilateral obstruction of a solitary functioning kidney)
Harrison's Principles of Internal Medicine, 18e
Past History2014
Increased O2 demand suddenly NG decompression: about 2600-3300ml/day Suspected septic shock
Mar, 04
Mar, 05 Consult nephrologist; transfer to MICU? DNR(+)
Mar, 05Mar, 05
Family decided to discontinue inotropic agents Passed away
Mar, 06
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
Discussion--1. Metabolic alkalosis
2. The rule of dialysis for treatment for severe metabolic alkalosis
Metabolic alkalosis
F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135
F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135
F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135
F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135
SCNN1B geneKCNJ1 gene
HSD11B2 gene
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
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
F. John Gennari, Am J Kidney Dis, Vol 55, No 6 (June), 2010: pp 1130-1135
Genetic analysis: gold standard Aldosterone antagonist: for 11HSD2
deficiency; no effect to Liddle syndrome Amiloride: blocks ENaC directly,
treatment for Liddle syndrome
Clinical course of a patient with CHF and metabolic
alkalosis
Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827
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
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
Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827
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
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
Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827
Aldo J. Peixoto, Am J Kidney Dis. 2013;61(5):822-827
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
The rule of dialysis for treatment for severe metabolic alkalosis
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
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
Lu Huber, Am J Kidney Dis. 2011;58(1):144-149
iHD 2hoursNG
4700ml iHD
Lu Huber, Am J Kidney Dis. 2011;58(1):144-149
Lu Huber, Am J Kidney Dis. 2011;58(1):144-149
+
Lu Huber, Am J Kidney Dis. 2011;58(1):144-149
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
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
Lu Huber, Am J Kidney Dis. 2011;58(1):144-149
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
Thank you for your attention!