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查 房 教 學
C A S E C O N F E R E N C E O F
I N T E R N A L M E D I C I N E
報告⼈人:Intern 1 陳佳菁
NYMUH, 2017/08/16
PART01
Patient Profile, Chief Complaint
History of Present Illness
PART02
Past Medical History, Family and Personal History,
Review of Systems, Physical Examination
PART03
Assessment
Plan
PART04
Mini-Topic
CONTENTS
ABOUT HIM
1
A 45 year-old man, with a history of
Hypertension / Type II DM/ Hyperlipidemia, who
presents with a chief complaint of epigastralgia
with nausea and vomiting for 1 day
M R . TA N G ,
Mr. Tang has a history of hypertension,
Type II DM, Hyperlipidemia. He was in his
usual state of health until several hours
prior to admission to NYMUH when he was
presented with epigastralgia, nausea, and
vomiting.
I S T O R Y O F P R E S E N T I L L N E S S
H
H P I M A N A G E M E N T
H P I M A N A G E M E N T
2
Past Medical History, Family and Personal History,
Review of Systems, Physical Examination
P A R T
CASE CONFERENCE 2017/08/16
MEDICAL HISTORY
PAST
Surgical, Medical History and Medication
?H I S T O R Y
1991 / 1994, L2-3-4-5 HIVD Operation
2006, Appendectomy
2016, Fasciectomy for cellulitis over left lower extremity
SURGICAL
W I T H O U T A D V E R S E E F F E C T O F A N E S T H E S I A O R B L O O D T R A N S F U S I O N
MEDICATION
PMH
Family members -
Father - Hypertension, DM
HISTORY
FAMILY
No common disease runs in his family
Mr. Tang, a chef, could perform
ADL and IADL independently.
HISTORY
PERSONAL
‣ Cigarette: 1 pack per day for 30 years
‣ Alcohol: Nil
‣ Drug abuse: Nil
‣ Betel nuts: Nil
‣ No TOCC
REVIEW
General - Left lower leg pain, (-)Weight change, (-)Fatigue, (-)Fever, (-)Weakness

HEENT - (-)Headache, (-)Dizziness, (-)Rhinorrhea, (-)Nasal Congestion, (-)Sore throat

Cardiovascular - (-)Chest pain, (-)Dyspnea, (-)Palpitation

Respiratory - (-)Cough, (-)Sputum, (-)Tachypnea

Gastrointestinal - (+)Epigastralgia, (+)Nausea, (+)Vomiting, (-)Dysphagia, (-)Diarrhea,
(-)Constipation

Genitourinary - (-)Frequency, (-)Urgency, (-)Hesitancy, (-)Dysuria, (-)Hematuria
OF SYSTEMS ,
A
General Appearance 

No cardiopulmonary distress
B
Vital Signs

T/P/R: 35.8C / 72 bpm / 18/min, BP: 150/103 mmHg

BW: 51.8kg
C
Heart

Inspection: No jugular vein engorgement

No murmurs, RHB

No tachycardia or bradycardia

No S3, S4 gallop
D Chest

Symmetrical expansion of chest wall

Breath sounds: Normal

Palpation / Percussion: Normal
PHYSICAL EXAMINATION
E
Abdomen 

Inspection: No spider angioma or scar

Auscultation: Normactive bowel sound

Palpation: Normal
F
Neurology

Motor function: Normal ROM

Sensation: Intact
G
Hemogram

HGB 12.5 g/dl, HCT 34.7%, PLT 196,000/ul

WBC 9,990/ul, SEG 75.9%
H
BCS

Glucose 149 mg/dl, CRP 1.44

CK-MB 9.8 U/L, CK 136 U/L, Troponin I < 0.1

TBIL 0.78 mg/dl, ALP 67 U/L

BUN 44 mg/dl, Creatinine 5.24 mg/dl

Amylase 40 U/L; ALT 20 U/L

Na 138 mmol/L, K 4.4 mmol/L
PHYSICAL EXAMINATION
P A R T
3
A S S E S S M E N T
P L A N
PATIENT’S MAJOR PRESENTING PROBLEM IS
T
A C U T E R E N A L FA I L U R E 

W I T H U R E M I C S Y M P T O M S
HE
- G E N T L E H Y D R AT I O N A S N S 1 0 0 0 M L Q D
F O R A C U T E R E N A L FA I L U R E
- R E N A L E C H O O N 8 / 9
- A N T I E M E T I C A G E N T P R O M E R A N F O R
U R E M I C S Y M P T O M S
- S E L F P R E PA R E I N S U L I N A N D
A N T I H Y P E R T E N S I O N M E D I C AT I O N F O R
T Y P E 2 D M C O N T R O L
- P E S O N 8 / 1 4 D U E T O E P I G A S T R A L G I A
W I T H S U S P E C T G U
COURSE
HOSPITAL
V I TA L S I G N , P E , L A B , M A N A G E M E N T, P R O G R E S S
VITAL SIGN, BW, PULSE OXYGEN SATURATION
I N PAT I E N T C O U R S E
PRESCRIPTION
I N PAT I E N T C O U R S E
PRESCRIPTION
PRESCRIPTION
PRESCRIPTION
4
MINI-TOPIC
A C U T E K I D N E Y I N J U RY
PART04
AKI
A K I
INTRODUCTION
-AN ABRUPT DECLINE IN KIDNEY FUNCTION
-USUALLY REVERSIBLE DECLINE IN THE GLOMERULAR FILTRATION
RATE (GFR)
-ELEVATION: SERUM BLOOD UREA NITROGEN (BUN), CREATININE,
AND OTHER METABOLIC WASTE PRODUCTS
-POTENTIALLY LIFE-THREATENING COMPLICATIONS - VOLUME
OVERLOAD, HYPERKALEMIA, ACIDOSIS, AND UREMIA
INPATIENT
ACUTE TUBULAR NECROSIS
OTHERS
Ischemia
Nephrotoxin Exposure
Sepsis
Volume Depletion
Urinary Obstruction
Rapidly Progressive
Glomerulonephritis
Acute Interstitial Nephritis
PATHOGENESIS
❖ Hypovolemic - Acute hemorrhage / Diarrhea /
Unreplenished insensible losses
❖ Hypervolemic - HFrEF
❖ Renal vascular autoregulation - afferent arteriole
vasoconstriction NSAIDs
PRERENAL
❖ Nephritic - proliferative glomerulonephritis; active
urine sediment with dysmorphic red cells and white
cells; granular, red cell, and other cellular casts; and
a variable degree of proteinuria. e.g. Rapidly
progressive glomerulonephritis (RPGN)
❖ Nephrotic - Rare in hospitalization patient
INTRINSIC GLOMERULAR DZ
❖ Most common - ATN, typically occurring following
radiocontrast or other nephrotoxin administration,
following cardiac surgery, or in the setting of sepsis or
shock
❖ Acute interstitial nephritis (AIN; which is often drug
induced) and cast nephropathy in multiple myeloma
INTRINSIC TUBULAR & INTERSTITIAL DZ
❖ Tumor lysis syndrome (acute urate nephropathy)
@high tumor burden lymphoma or following C/T
❖ Crystalline nephropathy associated with acyclovir and
other medications
❖ Acute phosphate nephropathy following a phosphate-
containing bowel preparation
INTRINSIC TUBULAR & INTERSTITIAL DZ
❖ Both small-and large-sized blood vessels
❖ Acute, small - small vessel vasculitides and diseases
that cause microangiopathy and hemolytic anemia
(MAHA), including thrombotic thrombocytopenic
purpura-hemolytic uremic syndrome (TTP/HUS),
scleroderma, atheroembolic disease, and malignant
hypertension
INTRINSIC RENAL VASCULAR DZ
❖ Both small-and large-sized blood vessels
❖ Acute, large - renal infarction from aortic dissection,
systemic thromboembolism, or renal artery
abnormality (such as aneurysm) and acute renal vein
thrombosis
INTRINSIC RENAL VASCULAR DZ
❖ No CKD - GFR substantial reduction ☛ Bil.
obstruction; Cause: Prostate Dz / Metastatic cancer
❖ Retroperitoneal fibrosis - Rare
❖ Untreated ☛ Irreversible tubulointerstitial fibrosis
OBSTRUCTIVE UROPATHY
A K I
VOLUME DEPLETION
-CLINICAL HX + PE HYPOVOLEMIA + OLIGURIA ☛ IV FLUID ADMINI.
-CRYSTALLOID SOLUTIONS, NON-POTASSIUM-CONTAINING
-PHYSIOLOGIC ENDPOINTS: MAP, URINE OUTPUT, CO
-RESPOND TO ADMINISTERED VOLUME ☛ PRERENAL? ATN?
A K I
VOLUME OVERLOAD
-ATN, ILL ☛ ANTI / BLOOD / IV DRUG / NUTRITION
-VOLUME EXPANSION, PULMONARY EDEMA
-DIURETICS, NOT PROLONG TO POSTPONE DIALYSIS
-LOOP DIURETICS, NATRIURETIC! IV FUROSEMIDE 40-80 MG
A K I
HYPERKALEMIA
-OLIGURIC PT, ESP. RHABDOMYOLYSIS, TUMOR LYSIS SYNDROME
-FEW S/S; VERY HIGH ☛ NEUROMUSCULAR, CARDIAC CONDUCTION
-DIALYSIS, UNLESS MILD HYPERKALEMIA <5.5, REVERSIBLE
-MEMBRANE, EC ☛ IC, OUT OF BODY
THANKS
C H I A - C H I N G , C H E N
F O R Y O U R L I S T E N I N G A N D C O M M E N T S

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[20160816][Case Presentation][Acute Kidney Injury][Chen, Chia Ching]

  • 1. 查 房 教 學 C A S E C O N F E R E N C E O F I N T E R N A L M E D I C I N E 報告⼈人:Intern 1 陳佳菁 NYMUH, 2017/08/16
  • 2. PART01 Patient Profile, Chief Complaint History of Present Illness PART02 Past Medical History, Family and Personal History, Review of Systems, Physical Examination PART03 Assessment Plan PART04 Mini-Topic CONTENTS
  • 3. ABOUT HIM 1 A 45 year-old man, with a history of Hypertension / Type II DM/ Hyperlipidemia, who presents with a chief complaint of epigastralgia with nausea and vomiting for 1 day M R . TA N G ,
  • 4. Mr. Tang has a history of hypertension, Type II DM, Hyperlipidemia. He was in his usual state of health until several hours prior to admission to NYMUH when he was presented with epigastralgia, nausea, and vomiting. I S T O R Y O F P R E S E N T I L L N E S S H
  • 5. H P I M A N A G E M E N T
  • 6. H P I M A N A G E M E N T
  • 7. 2 Past Medical History, Family and Personal History, Review of Systems, Physical Examination P A R T CASE CONFERENCE 2017/08/16
  • 8. MEDICAL HISTORY PAST Surgical, Medical History and Medication
  • 9. ?H I S T O R Y 1991 / 1994, L2-3-4-5 HIVD Operation 2006, Appendectomy 2016, Fasciectomy for cellulitis over left lower extremity SURGICAL W I T H O U T A D V E R S E E F F E C T O F A N E S T H E S I A O R B L O O D T R A N S F U S I O N
  • 11. Family members - Father - Hypertension, DM HISTORY FAMILY No common disease runs in his family
  • 12. Mr. Tang, a chef, could perform ADL and IADL independently. HISTORY PERSONAL ‣ Cigarette: 1 pack per day for 30 years ‣ Alcohol: Nil ‣ Drug abuse: Nil ‣ Betel nuts: Nil ‣ No TOCC
  • 13. REVIEW General - Left lower leg pain, (-)Weight change, (-)Fatigue, (-)Fever, (-)Weakness
 HEENT - (-)Headache, (-)Dizziness, (-)Rhinorrhea, (-)Nasal Congestion, (-)Sore throat
 Cardiovascular - (-)Chest pain, (-)Dyspnea, (-)Palpitation
 Respiratory - (-)Cough, (-)Sputum, (-)Tachypnea
 Gastrointestinal - (+)Epigastralgia, (+)Nausea, (+)Vomiting, (-)Dysphagia, (-)Diarrhea, (-)Constipation
 Genitourinary - (-)Frequency, (-)Urgency, (-)Hesitancy, (-)Dysuria, (-)Hematuria OF SYSTEMS ,
  • 14. A General Appearance 
 No cardiopulmonary distress B Vital Signs
 T/P/R: 35.8C / 72 bpm / 18/min, BP: 150/103 mmHg
 BW: 51.8kg C Heart
 Inspection: No jugular vein engorgement
 No murmurs, RHB
 No tachycardia or bradycardia
 No S3, S4 gallop D Chest
 Symmetrical expansion of chest wall
 Breath sounds: Normal
 Palpation / Percussion: Normal PHYSICAL EXAMINATION
  • 15. E Abdomen 
 Inspection: No spider angioma or scar
 Auscultation: Normactive bowel sound
 Palpation: Normal F Neurology
 Motor function: Normal ROM
 Sensation: Intact G Hemogram
 HGB 12.5 g/dl, HCT 34.7%, PLT 196,000/ul
 WBC 9,990/ul, SEG 75.9% H BCS
 Glucose 149 mg/dl, CRP 1.44
 CK-MB 9.8 U/L, CK 136 U/L, Troponin I < 0.1
 TBIL 0.78 mg/dl, ALP 67 U/L
 BUN 44 mg/dl, Creatinine 5.24 mg/dl
 Amylase 40 U/L; ALT 20 U/L
 Na 138 mmol/L, K 4.4 mmol/L PHYSICAL EXAMINATION
  • 16. P A R T 3 A S S E S S M E N T P L A N
  • 17. PATIENT’S MAJOR PRESENTING PROBLEM IS T A C U T E R E N A L FA I L U R E 
 W I T H U R E M I C S Y M P T O M S HE
  • 18. - G E N T L E H Y D R AT I O N A S N S 1 0 0 0 M L Q D F O R A C U T E R E N A L FA I L U R E - R E N A L E C H O O N 8 / 9 - A N T I E M E T I C A G E N T P R O M E R A N F O R U R E M I C S Y M P T O M S - S E L F P R E PA R E I N S U L I N A N D A N T I H Y P E R T E N S I O N M E D I C AT I O N F O R T Y P E 2 D M C O N T R O L - P E S O N 8 / 1 4 D U E T O E P I G A S T R A L G I A W I T H S U S P E C T G U
  • 19. COURSE HOSPITAL V I TA L S I G N , P E , L A B , M A N A G E M E N T, P R O G R E S S
  • 20. VITAL SIGN, BW, PULSE OXYGEN SATURATION
  • 21. I N PAT I E N T C O U R S E
  • 22. PRESCRIPTION I N PAT I E N T C O U R S E
  • 26.
  • 27. 4 MINI-TOPIC A C U T E K I D N E Y I N J U RY PART04 AKI
  • 28. A K I INTRODUCTION -AN ABRUPT DECLINE IN KIDNEY FUNCTION -USUALLY REVERSIBLE DECLINE IN THE GLOMERULAR FILTRATION RATE (GFR) -ELEVATION: SERUM BLOOD UREA NITROGEN (BUN), CREATININE, AND OTHER METABOLIC WASTE PRODUCTS -POTENTIALLY LIFE-THREATENING COMPLICATIONS - VOLUME OVERLOAD, HYPERKALEMIA, ACIDOSIS, AND UREMIA
  • 29. INPATIENT ACUTE TUBULAR NECROSIS OTHERS Ischemia Nephrotoxin Exposure Sepsis Volume Depletion Urinary Obstruction Rapidly Progressive Glomerulonephritis Acute Interstitial Nephritis PATHOGENESIS
  • 30.
  • 31. ❖ Hypovolemic - Acute hemorrhage / Diarrhea / Unreplenished insensible losses ❖ Hypervolemic - HFrEF ❖ Renal vascular autoregulation - afferent arteriole vasoconstriction NSAIDs PRERENAL
  • 32.
  • 33. ❖ Nephritic - proliferative glomerulonephritis; active urine sediment with dysmorphic red cells and white cells; granular, red cell, and other cellular casts; and a variable degree of proteinuria. e.g. Rapidly progressive glomerulonephritis (RPGN) ❖ Nephrotic - Rare in hospitalization patient INTRINSIC GLOMERULAR DZ
  • 34. ❖ Most common - ATN, typically occurring following radiocontrast or other nephrotoxin administration, following cardiac surgery, or in the setting of sepsis or shock ❖ Acute interstitial nephritis (AIN; which is often drug induced) and cast nephropathy in multiple myeloma INTRINSIC TUBULAR & INTERSTITIAL DZ
  • 35. ❖ Tumor lysis syndrome (acute urate nephropathy) @high tumor burden lymphoma or following C/T ❖ Crystalline nephropathy associated with acyclovir and other medications ❖ Acute phosphate nephropathy following a phosphate- containing bowel preparation INTRINSIC TUBULAR & INTERSTITIAL DZ
  • 36. ❖ Both small-and large-sized blood vessels ❖ Acute, small - small vessel vasculitides and diseases that cause microangiopathy and hemolytic anemia (MAHA), including thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP/HUS), scleroderma, atheroembolic disease, and malignant hypertension INTRINSIC RENAL VASCULAR DZ
  • 37. ❖ Both small-and large-sized blood vessels ❖ Acute, large - renal infarction from aortic dissection, systemic thromboembolism, or renal artery abnormality (such as aneurysm) and acute renal vein thrombosis INTRINSIC RENAL VASCULAR DZ
  • 38.
  • 39. ❖ No CKD - GFR substantial reduction ☛ Bil. obstruction; Cause: Prostate Dz / Metastatic cancer ❖ Retroperitoneal fibrosis - Rare ❖ Untreated ☛ Irreversible tubulointerstitial fibrosis OBSTRUCTIVE UROPATHY
  • 40.
  • 41.
  • 42.
  • 43.
  • 44.
  • 45. A K I VOLUME DEPLETION -CLINICAL HX + PE HYPOVOLEMIA + OLIGURIA ☛ IV FLUID ADMINI. -CRYSTALLOID SOLUTIONS, NON-POTASSIUM-CONTAINING -PHYSIOLOGIC ENDPOINTS: MAP, URINE OUTPUT, CO -RESPOND TO ADMINISTERED VOLUME ☛ PRERENAL? ATN?
  • 46. A K I VOLUME OVERLOAD -ATN, ILL ☛ ANTI / BLOOD / IV DRUG / NUTRITION -VOLUME EXPANSION, PULMONARY EDEMA -DIURETICS, NOT PROLONG TO POSTPONE DIALYSIS -LOOP DIURETICS, NATRIURETIC! IV FUROSEMIDE 40-80 MG
  • 47. A K I HYPERKALEMIA -OLIGURIC PT, ESP. RHABDOMYOLYSIS, TUMOR LYSIS SYNDROME -FEW S/S; VERY HIGH ☛ NEUROMUSCULAR, CARDIAC CONDUCTION -DIALYSIS, UNLESS MILD HYPERKALEMIA <5.5, REVERSIBLE -MEMBRANE, EC ☛ IC, OUT OF BODY
  • 48. THANKS C H I A - C H I N G , C H E N F O R Y O U R L I S T E N I N G A N D C O M M E N T S