ANESTHESIA FOR A PATIENT WITH CHRONIC

KIDNEY DISEASE UNDERGOING EXPLORATORY

LAPROTOMY DUE TO ABDOMINAL MASS
Dr Samra Ahmad
UKSO
AP Dr Naeem Sheikh
 OBJECTIVES
At the end of the presentation we will be able to learn
• Chronic Kidney Disease Etiology
• Classification
• Pathophysiological consequences of CKD
• History taking in a CKD patient
• Examination of a CKD patient
• Relevant Investigations
• Optimization of patient with CKD
• Impact Of abdominal mass on anesthesia
• Factors affecting Renal Blood Flow
• pharmacokinetic & dynamics of drugs in CKD
• Induction of anesthesia in CKD
• Analgesia in a CKD patient with abdominal mass
CASE SCENARIO
A 58 year old male hypertensive patient from last 10 years with a
history of CKD since 5 years is scheduled for elective exploratory
laparotomy for CA colon
How will you proceed with this patient?
• History
• Examination
• Investigation
• Pre op evaluation and preparation
• Intra op management
• Post op management
 MEDICATION
• Amlodipine10 mg OD
• Rosuvastatin 10 mg HS
• Tab Calcium Carbonate 1250 mg PO TDS
• Inj Erthropoietin 3 x week
 EXAMINATION
• GPE
• Airway examination
• CVS
• Respiratory
VITALS
• BP 140/90 mmHg Weight 75 kg
• PR 89 bpm UOP 2 litres /day
• SPO2 97 % @ RA
• Temp 98.1 F
• RR 18 /min
GPE
• Pallor
• puffiness around eyes
• No pedal edema
CVS S1 + S2, JVP normal
CHEST NVB no added sounds
PA Soft ,non tender, mass papable in RHC,bowel sound audible
CNS well oriented in time and place GCS 15/15
Airway Examination
• Mallampati class 2
• Interincisor gap 4 cm
• Thyromental distance . 6cm
• Sternomental distance 12 cm
‫?‪How will you take history of this patient‬‬
‫السالم علیکم میرا نام ڈاکٹر ———‪ -‬ہے میں بیہوشی کے شعبے سے تعلق ہے مجھے آپ سے اپ‬
‫کے آپریشن سے پہلے بیہوشی دینے کےلیے کچھ سواالت پوچھنے ہیں ہے‬
‫اس کیلے مجھکو آپ کا تعاون درکار ہے‬
‫‪Demographic‬‬
‫آپ کا کیا نام ہے؟‬

‫ت‬
‫آپ کی کیا عمر ہے ؟‬
‫آپ ک ی ا کام کرے ہ ی ں؟‬

‫‪Surgical Hx‬‬
‫آپ یہاں کس چیز کے آپریشن کیلے آئے ہیں؟‬
‫آپ کو اس مسئلے کی کیا عالمات تھیں؟‬
‫پ کا پہلے کوئ آپریشن تو نہیں ہوا؟‬
 ‫ئ‬ ‫ت‬ ‫ئ‬
‫ے کے سا ھ ی ہاںت آے ہ ی ں؟‬ ‫آپ کس مس ل‬
‫سئ‬
‫المات ھی ں؟ ت‬ ‫ع‬ ‫ے کی ک ا‬ ‫آپ کو اس م ل‬
‫یگ ٹ ت ن‬
‫آپ کو کوئ رسولی ی ا ل ی و ہی ں محسوس ہ و ی؟‬
‫ے؟‬ ‫رسولی کب سے ہ‬
‫آپ کو ک س ت‬
‫ے؟‬ ‫ے پ ہ لگا تکہ آپ کے پ ی ٹ می ں رسولی ہ‬ ‫ی‬
‫ت‬
‫ک ی ا آپ کا وزن کم ہ و ا ھا؟‬
‫ٹ ن‬
‫ے؟‬ ‫ے کی رسولی کا ب ت ای ا ہ‬‫آپ کو ڈاک قر ے پ ی ٹ کے کس حص‬
‫ہت‬ ‫ت ن‬
‫ک ی ا آپ کو ب ض و ہی ں ر ی؟‬
‫ن‬ ‫ت خ‬
‫ک ی ا آپ کا پ ی ٹ و راب تہی ں رہ ت ا؟‬
‫ت ن‬ ‫ٹ‬
‫ک ی ا آپ کو ال ی اں و ہی ںت آ نی؟ ت‬
‫ک ی ا آپ کو پ ی ٹ می ں درد و ہی ں ہ و ی؟‬
‫ن‬
‫ے؟‬ ‫الج کروای ا ہ‬ ‫ک ی ا آپ ے اس کا کوئ ع‬
‫ت ن‬
‫ے سے ب ڑی و نہی ں ہ و رہ ی؟‬ ‫ک ی ا ی ہ رسولی پہل‬
‫ج ش ت ن‬ ‫کئ ش ئ‬
‫ے؟‬ ‫ل‬ ‫ک‬ ‫ی‬
‫ے عا ی ں ی ا ا ن و ہی ں گ‬
‫ت‬ ‫ن‬ ‫ت‬ ‫ک ی ا آپ کو اس ی ل‬
‫ے می ں سوج ن قو محسوس ہی ں ہ و ی؟‬ ‫ک ی ا آپ کو پ ی ٹ کے کسی حص‬
‫ض‬ ‫ٹ ن‬
‫ے کہ ی ہ رسولی ب ا ی اع اء پر دب او ڈال رہ ی ہ‬
‫ے‬ ‫ک ی ا آپ کو ڈاک ر ے ب ت ای ا ہ‬
 ‫ن‬
‫آپ کو اس کے عالوہ کوئ مسئ لہت و ہی ں‬
‫ے؟‬‫ہ‬
‫‪HTN:‬‬
‫کیا ٓاپکو بلڈ پریشر کا مٗس لہ ہے‬
‫ئ‬ ‫ش‬
‫کب سے ب لڈ پری ر کا مس لہ تہ‬
‫ے؟‬ ‫ش ئ‬
‫کو‬ ‫آپ‬
‫ے‬ ‫ے آپ کون سی دوائ اس عمال کر رہ‬ ‫ب لڈ پری ر ک ی ل‬
‫ہ ی ں؟‬
‫ے ہ ی ں؟‬ ‫کب سے دوائ کھا رہ‬
‫ٹ‬ ‫ش ن‬
‫ے؟‬ ‫ہ‬ ‫ک ی ا آپ کا ب لڈ پری ر ک رول رہ ت ا‬
‫ئ ت ن‬ ‫ن‬
‫ے؟‬ ‫ہ‬ ‫ں‬ ‫ی‬ ‫ہ‬ ‫و‬ ‫لہ‬ ‫س‬ ‫م‬ ‫کوئ‬ ‫کا‬ ‫ھوں‬ ‫ک ا آپ کو آ ک‬
‫ت‬ ‫ت ن‬ ‫ت‬ ‫ی‬
‫پن‬
‫ں و ی؟‬‫ہ‬ ‫م‬ ‫ہ‬ ‫ہ‬
‫سوس و ہی ت‬
‫ت ح ن‬
‫ک ی ا آپ کو ا ی ب ی ن ائ کم و ی وئ‬
‫ک ی ا آپ کو کب ھی ج سم می ں کمزوری و محسوس ہی ں ہ و ی؟‬
‫ت ن‬ ‫ٹ‬ ‫کب ف‬
‫ہ‬
‫ک ی ا آپ کو ھی ا تلج کا ا ی ک و ہی ں وا؟‬
‫ئ ت ن‬ ‫ت نئ‬
‫ک ی ا آپ کو کب ھی چ ھا ی می ں درد و ی ں ہ وئ؟ک ی ا آپ کو دل کا کوئ مس لہ و ہی ں ہ وا؟‬
‫ئ ت ن‬
‫ک ا آپ کو کب ھی گردوں کا مس لہ و ہی ں ہ وا؟‬
 ‫‪:Renal disease‬‬
‫ے؟‬ ‫سے‬ ‫کب‬ ‫لہ‬ ‫آپ کو گردوں کا س ئ‬
‫ہ‬ ‫نم‬
‫خ‬
‫ے؟‬ ‫گردے راب وے کے ک ی ا وج ہ ہ‬ ‫ہ‬
‫ئ‬ ‫ت‬
‫ے؟‬
‫ے پرہ لگا ھا ٹکہ آپ کو گردوں کا مس لہ ہ‬ ‫آپ کو کی س‬
‫ت‬ ‫خ‬
‫ک ی ا آپ کا ون کا کوئ ی سٹ ہ وا ھا؟‬
‫ت‬ ‫ئ‬ ‫ش‬ ‫ق‬
‫اب کا کوئ مس لہ ہ وا ھا؟‬ ‫آپ کو پ یت ت‬ ‫ک ی ا اس و ت‬
‫ت ن‬ ‫خ‬
‫ون ی ا ج ھاگ و ہی ں آ ی ھی؟‬
‫ت ت‬ ‫خ ٹ‬ ‫ام‬
‫ھا؟‬ ‫گا‬ ‫ہ‬ ‫پ‬ ‫ں‬ ‫ی‬‫م‬ ‫سٹ‬ ‫ی‬ ‫ون‬ ‫کے‬ ‫مول‬‫ع‬ ‫ی‬
‫ت‬ ‫لت ن‬ ‫خ‬ ‫ش‬
‫ک ی ا آپ کو پ ی اب می ں ون ی ا ج ھاگ و ہی ں آ ی؟‬
‫کبھی صبح اٹھ کے منہ پے یا آنکھوں کے گرد سوج تو نہيں پڑی ہوتی؟‬
‫پيشاب جل کے تو نہيں آتا؟‬
‫پيشاب کرتے وقت درد تو نہيں ہوتی؟‬
‫ئ سئ ت ن‬ ‫ت‬ ‫ت خ ت ن‬ ‫ش‬ ‫کب‬
‫ے؟‬
‫ہ‬ ‫ں‬ ‫ي‬ ‫ہ‬ ‫و‬ ‫ہ‬ ‫ل‬ ‫م‬ ‫ی‬ ‫کو‬ ‫کا‬ ‫گردوں‬ ‫کو‬ ‫آپ‬ ‫ا۔‬ ‫آ‬ ‫ں‬ ‫ي‬ ‫ہ‬ ‫و‬ ‫ون‬ ‫ھ‬ ‫سا‬ ‫کے‬ ‫اب‬ ‫ي‬ ‫پ‬ ‫ھی‬
 ‫ت‬ ‫ت ن‬ ‫ش‬
‫ک ی ا آپ کو پ ی اب کم ی ا زی ادہ و ہی ں آ ا؟‬
‫ت‬ ‫ن‬ ‫ت ت‬
‫ک ی ا آپ درد کی دوائ ی اںت و اس عمال ہی ں کرے؟‬
‫ٹ ت ن‬
‫آپ کو ال ی و ہی ں آ ی؟‬
‫ت‬ ‫ن‬ ‫ت خ‬
‫ا؟‬ ‫و‬ ‫ی ا دل و راب ہی ں ہ‬
‫ت‬ ‫ت ن‬
‫ی؟‬ ‫و‬ ‫آپ کو جسم پر خ ارش و ہی ں ہ‬
‫ت‬ ‫ت ن‬ ‫ت‬ ‫پٹ‬
‫آپ کو نھں ی ا ج سم می ں درد ی ا ھکاوٹ و ہی ں ہ و ی؟‬
‫ت ن‬
‫آپ کا سا س و ہی ں پ ھولت ا؟‬
‫ت‬ ‫ت‬ ‫ن ت‬ ‫لن‬
‫ے ا عمال کرے ہ ی ں؟‬ ‫س‬ ‫ے کی‬ ‫ے تک‬ ‫ک‬ ‫ے‬
‫ن‬ ‫ت‬ ‫ن‬ ‫ی ٹ ی لی‬
‫کھ ت‬
‫رات کو آ کھ و ہی ں ل ی؟‬
‫ع‬ ‫سئ ک ئ‬ ‫ن‬
‫ے ہ ی ں؟‬
‫ے ک ی ا الج کروا رہ‬ ‫ے یل‬ ‫م‬
‫ے گردوں کے ل‬ ‫آپ ا پ‬
 ‫خ‬ ‫ت ن‬ ‫ن‬ ‫غ‬
‫کی حالت نمی ں ہ سپ ت ال و ہی ں دا ل ہ وے؟‬ ‫ک ی ا آپ کب ھی ودگی فن‬
‫ن ت ن‬ ‫یش‬ ‫ت‬
‫ک ی ا آپ کو کب ھی چ ھا ی کا ا ک ن ی ا مو ی ا و ہی ں ہ وا؟‬
‫ت‬ ‫ت ن‬ ‫ن‬
‫ک ی ا آپ کو کھا ا کھا کر معدہ ب ھاری و ہی ں ہ و ا؟‬
‫ن ہض ن‬ ‫ت‬ ‫ت ن‬ ‫ہ‬
‫ہ‬ ‫ک‬ ‫ہ‬
‫ک ی ا آپ کو ایسا حسوس و ہی ں و ا کہ ھا ا م ہی ں وا؟‬
‫ئ‬ ‫ت‬ ‫ٹ ن‬
‫ک ی ا آپ کو ڈاک ر ے ب ت ای ا ھا کہ آپ کو گردوں کا مس لہ یک وں ہ وا ؟‬
‫ت‬ ‫ت ن‬ ‫ت‬
‫ک ی ا آپ ج ب کھڑے ہ وے ہ ی ں آپ کو چ کر و ہی ں آے؟‬
‫ت‬ ‫ٹ ت ن‬ ‫ع کئ‬
‫ے؟‬‫ے و ہی ں لگ‬ ‫ے آپ کو کوئ ی ک‬ ‫ک ی ا گردے کے الج ی ل‬
 ‫ئ‬ ‫فئ‬
‫ے ہیں ؟‬ ‫گردوں کی ص ا ی ‪ /‬ڈا لسز کروا رہ‬ ‫آپ‬
‫کن ت ئ‬ ‫ہ فت‬
‫ے ہیں ؟‬ ‫آپ ے می ں کب اور ت ی مر ب ہ ڈا لسز سے کروا رہ‬
‫ئ‬
‫ے ہ ی ں؟‬ ‫ہ‬ ‫کون سا ڈا لسز کروا ر‬
‫ت‬ ‫ئ‬ ‫ن‬ ‫کن‬
‫ے؟‬‫ہ‬ ‫ہ‬
‫ے کا ڈا لسز و ا‬ ‫ے دورا ی‬ ‫ت‬
‫ش ت ن‬ ‫ئ‬
‫ہ‬ ‫ی‬
‫ے آپ کے ب ازو پر کوئ آپر ن و ہی ں وا؟‬ ‫ل‬ ‫اس کے‬
‫ش ٹ‬ ‫ل ئ‬ ‫ت ن‬
‫گردن می ں ی ا ب تازو می ں کوئ سوئ و ہی ں گی ڈا لسز کے دوران اور ب عد می ں ب لڈپری ر ھ ی ک رہ ت ا‬
‫ے؟‬ ‫ہ‬ ‫ے؟ ی ا بڑھ ج ا ا‬ ‫ہ‬
‫ت‬ ‫کن ت پ ش‬
‫ے؟‬ ‫آپ کو دنن می ں ت ئی مر ب ہ ی اب آ ا ہ‬
‫پ ت‬ ‫ن‬ ‫ت‬
‫ے ہ ں؟‬ ‫ی‬ ‫آپ ک ا پ ا ی‬
‫ن‬ ‫غ ت ت‬ ‫خ‬
‫ے؟‬ ‫س‬
‫ک ی ا آپ کوئ اص ذا و انعمال ہی ں کر رہ‬
‫ے؟‬ ‫وئ‬ ‫ہ‬ ‫ئ‬ ‫دی‬ ‫ت‬ ‫دا‬ ‫کی‬ ‫ے‬ ‫کر‬ ‫ل‬ ‫د‬ ‫ا آپ کو گردے ت‬
‫ہ‬ ‫گ‬ ‫ی‬ ‫ہ‬ ‫ی‬ ‫ب‬ ‫کی‬
 ‫‪DM:‬‬
‫آپ کو پياس زیادہ تو نہيں لگتی؟‬
‫آپ کو پيشاب زیادہ تو نہيں آتا؟‬
‫آپ کو رات کو پيشاب کے ليے بار بار اٹھنا تو نہيں پڑھتا؟ ‪-‬‬
‫آپ کو شوگر کا مسلئہ تو نہيں ہے؟‬
‫‪IHD:‬‬
‫آپ کو کبھی سينے ميں درد یا گٹھن تو نہيں محسوس ہوئی؟‬
‫آپ کو کبھی سينے ميں درد یا گٹھن ک آپ کو کبھی دل کا کوئی مسلئہ تو نہيں ہوا؟‬
‫آپ کو کبھی دل کا اٹيک تو نہيں ہوا؟‬
‫‪CVA:‬‬
‫آپ کو جسم کے کسی خصے کی کمزوری‬
‫تو نہيں ہوئی کبھی؟ آپ کے جسم کا کوئی حصہ سن تو نہيں ہوتا؟‬
‫آپ کو کبھی فالج کا اٹيک تو نہيں ہوا؟‬
‫‪Asthma:‬‬
‫کبھی سانس کے ساتھ سيٹی کی آواز تو نہيں آتی؟ آپ کو کبھی دمہ کا مسلئہ تو نہيں ہوا؟‬
 ‫‪Dyspnea:‬‬
‫آپ کا سانس تو نہيں پھولتا؟‬
‫اپنے کام آسانی سے کر ليتے ہيں؟‬
‫‪orthopnea:‬‬
‫کیا آ کو سيدھا ليٹ کے سانس کا مسلئہ تو نہيں ہوتا؟‬
‫کتنے تکيئے لے کر سوتے ہيں؟‬
‫‪PND‬‬
‫بھی رات کو سوتے وقت سانس کا کوئی مسلئہ تو نہيں ہوا؟‬
‫کبھی سوتے ہوئے آنکھ کھل جائے اور لگے کے سانس نہيں آ رہا ميں کھڑکی کھولو کہ تازہ ہوا آئے یا ميں تازہ ہوا ميں‬
‫باھر جائو‬
‫‪APD:‬‬
‫معدے ميں درد جلن تو نہيں ہوتی کھانا کھانے کے بعد؟‬
‫‪Smoking History:‬‬
‫کیا آپ سگریٹ تو نہیں پیتے‬
‫‪BLOOD TX HX‬‬
‫کیا آپ کو کبھی خون تو نہیں لگا ؟‬
 ‫‪Allergy:‬‬
‫کبھی کسی دوءائی سے الرجی تو نہيں ہوئی؟‬
‫کسی کھانے والی چيز سے الرجی تو نہيں ہوتی؟‬
‫‪joint disorders:‬‬
‫جوڑوں ميں درد تو نہيں ہے؟‬
‫گردن ميں درد تو نہيں ہوتا؟‬
‫‪OSA‬‬
‫آپ رات کو سوتے ہوئے کھراٹے تو نہيں مارتے؟‬
‫‪Liver disease:‬‬
‫آپ کو کبھی جگر کا مسلئہ تو نہيں ہوا؟‬
‫کبھی خون کی الٹی تو نہيں آ ئی؟‬
‫کالے رنگ کے پاہانے تو نہيں آتے؟‬
‫‪BLOOD TX HX‬‬
‫کیا آپ کو کبھی خون تو نہیں لگا ؟‬
‫اگر لگا ہے تو کس وجہ سے لگا؟‬
‫اگر لگاہے تو کیا آپ کو کبھی آپ کو ریکشن تو نہیں ہوا؟‬
What investigations will u advise & why ?
• FBC : Hb 9 g/dl
TLC 10
PLT 200000
• Electrolytes: Na 138
K5
Cl 100
• Coagulation :Normal
• ECG: NORMAL
• RFT : S.cret 2.5 mg/dl
UREA 70 mg/dl
• Serum Albumin : 3.3 mg /dl
• CXR : Normal
• CT Abdomen : colonic mass
 What is the ASA status of this patient?
• ASA III
PRESENT THE CASE OF THE PATIENT
• A 58 year old –male with 75 kg weight is a known hypertensive from last 10 years is
taking Amlodipine 10 mg once daily is compliant to his medication and his blood
pressure is controlled. He is diagnosed with CKD from last 5 years along with the
history of end organ damage like anemia ,autonomic neuropathy and hypo
albunemia. There is no history of dialysis. And he is in CKD stage 3b. He is scheduled
for elective exploratory laparotomy for CA Colon that was diagnosed 3 months back.
• His s.cret is 2.5mg/dl .urea 70. his K is 5 meq/l,and albumin is 3
• Rest of the labs are unremarkable
• On Examination he is vitally stable .
• His GPE shows pallor and periorbital edema .
On systemic examination a mass is palpable in RHC. rest of the systemic examination is
un remarkable .
What is Chronic Kidney Disease?
 Chronic Kidney Disease

• DEFINITION
• A kidney damage or abnormalities of kidney structure resulting in GFR
< 60 ml / min / 1.73 m2 for 3 months or more with progressive
inadequate ability of the kidney to perform its secretory, excretory &
regulatory function.
• < 40% of functioning nephrons.
What are the most common cause of CKD?
 Main causes of CKD
DM 40%
Hypertension 24 %
Glomerulonephritis 7%
Chronic Pyelonephritis 5%
Polycystic Renal Disease 4%
Others 20%
 Aetiology & risk factors for chronic kidney disease
Comorbids Vascular disease including renal vascular stenosis2
Hypertension
Type 2 diabetes mellitus
Intrinsic renal Glomerulonephritis
disease Acute kidney injury
Interstitial nephritis
Nephropathies Infective (e.g. pyelonephritis) Obstructive (e.g.
prostatic hypertrophy, nephrolithiasis) Reflux
Genetic Polycystic kidney disease
Alport syndrome
Fabry disease
Cystinosis

Metabolic Hypercalcaemia
Hyperparathyroidism causing nephrocalcinosis
Oxalosis
Neoplasm Myeloma
Renal tumour
Systemic disease Amyloidosis

Autoimmune Goodpasture syndrome

disease Scleroderma IgA
vasculitis
Systemic lupus erythematosus

Toxins Lead poisoning

Drug-related NSAID use nephropathy
Calcineurin inhibitors
Chemotherapeutic agents
others Haemolytic uraemic syndrome
Gout
Obstructive uropathy
How will you classify CKD?
 CLASSIFICATION OF CKD
• It is based on the GFR and the level of proteinuria
• GFR
 It is the volume of fluid filtered from the glomerular capillaries into
Bowman’s capsule per unit time
internationally accepted measure to express renal function.

• Value : 120 ± 25 mL/min in men

95 ± 20 mL/min in women.
• Clinical manifestation of CKD occurs : GFR < 25 mL/min.
Stages of renal dysfunction by GFR
Cockrofte Gault equation
(eCCr = estimated creatinine clearance)
 What is the CKD classification of this
patient?
Age 58 year .weight 75kg
• 34.17 ml/min
• G 3b- MODERATE SEVERE disease
What is the difference between CKD & CRF?
• CRF :GFR < 15 mL/min
 Pathophysiological Consequences in CKD
• Fluid & Electrolyte
• Hematological
• Coagulopathy
• Cardiovascular Abnormalities
• Pulmonary Abnormalities
• Gastrointestinal Abnormalities
• Neurological Abnormalities
• Immunological
• Endocrine
 FLUID & ELECTROLYTE

Hyponatremia:
Inability to excrete sodium & water
Increase hydrostatic pressure
Fluid moves in to Extracellular space
Hyperkalemia

Occurs at creatinine clearances of less than 5 mL/min2

large potassium loads due to drugs, trauma
Potassium secretion in the distal nephron is affected
K retention
DRUGS
• b-blockers
• potassium sparing diuretics (spironolactone)
• angiotensin converting enzyme (ACE) inhibitors or angiotensin antagonists
• NSAIDS
• aminoglycosides and cyclosporins
Hypermagnesemia
 decrease clearance
Increase intake eg Mg conataining antacids
Potentiate NDNMBs

Hypocalcemia

decreased kidney synthesis of 1,25-dihydroxycholecalciferol

decreased intestinal calcium absorption
hyperphosphatemia-associated calcium deposition into bone
Hypoalbuminemia
Increase protein losses
Anorexia, protein restriction, and dialysis
ACIDOSIS
• clearance of hydrogen ions is decreased
• increased production of non-volatile acids
• increased bicarbonate loss - reduced tubular bicarbonate reabsorption.
• inability to secrete protons or buffers and regenerate bicarbonate.
• Reduced utilization of glutamine
• decrease in ammonia production and secretion into the proximal tubule.
• Retention of organic anions causes a progressive increase in the anion
gap
• further fall in plasma bicarbonate concentration
 HEMATOLOGICAL

ANEMIA
• Occurs if creatinine clearance is below 30 mL/min
• normochromic normocytic anemia
• Causes
Decreased renal erythropoietin production - reduced stem cell transformation into
erythrocytes
Reduced red cell life span due to uremia
Dietary deficiency of iron and folate
Chronic upper GI tract losses
 Dialysis
Anemia Compensation

shift of the oxyhemoglobin dissociation curve to the right -increase 2, 3-

diphosphoglycerate production - increase oxygen delivery to the tissues
 increased cardiac output
 decreased viscosity increasing microcirculation
• Treatment: recombinant erythropoietin (EPO)
• Target hemoglobin 9.5 gm/dl
• A/E of EPO
hypertension
accelerated thrombosis
COAGULOPATHY
• Impaired qualitative function of Platelets
impaired release of von Willebrand factor/factor VIII complex-decrease binding and
activation of platelets
Dec ADP & impaired aggregation to ADP
platelets have decreased adhesiveness and aggregation
• increased release of β-thromboglobulin from platelets
• vascular production of PGI2
• Treatment
Cryoprecipitate/DDAVP (increases release of von Willebrand factor)
 DDAVP (0.3 mcg/kg)
Platelet transfusion – no role
CARDIOVASCULAR
• HYPERTENSION
 decreased blood oxygen-carrying capacity—CO increases.
 Sodium retention & fluid overload
abnormalities in the renin–angiotensin system
• CHF
• Pulmonary Edema- increased permeability of the alveolar– capillary
membrane
 Left Ventricular Hypertrophy
• Volume overload –
water and sodium retention
Treatment: diuretics- fluid restriction
 chronic anemia – hyperdynamic circulation - increased stroke volume
and tachycardia
• Pressure overload – hypertension and arteriosclerosis.
• myocardial fibrosis and impaired myocardial relaxation— diastolic
dysfunction
• Arrhythmias – metabolic derrangements
• Uremic pericarditis— pericardial tamponade – sudden death
 Ischemic heart disease
• Atherosclerosis
impaired triglyceride clearance & lipoprotein lipase activity- impaired
lipolysis.
RAS activation– production of ROS –endothelial dysfunction
Low grade inflammation
Treatment : statins
• Calcific vulvular heart lesions: hypocalcemia + hyperphosphatemia—
Calcium deposition in valves & small blood vessels
 PULMONARY
• Atelectasis- decrease surfactant production
• Pulmonary extravascular water is increased -- interstitial edema –
widening of the alveolar to arterial oxygen gradient – hypoxemia.
• Fluid overload –Increased permeability of the alveolar capillary
membrane -- pulmonary edema
• decrease in pulmonary compliance—reduced functional residual
capacity– ventilation perfusion mismatch.
• Restrictive pulmonary dysfunction
 GASTROINTESTINAL
• Anorexia, nausea, vomiting and ileus— uremia
• Uremia - mucosal irritation— gastrointestinal tract bleeding
• Hypersecretion of gastric acid - peptic ulceration
• Delayed gastric emptying – autonomic neuropathy -- perioperative
aspiration.
• hepatitis B and C--hepatic dysfunction
 ENDOCRINE
• secondary hyperparathyroidism
hypocalcemia and hyperphosphatemia
increases the osteoclast and osteoblast activity --Osteitis Fibrosa Cystica
• abnormal glucose tolerance -- peripheral insulin resistance
• Abnormalities in lipid metabolism– hypertriglyceridemia--
atherosclerosis.
• Increased circulating levels -- parathyroid hormone, insulin, glucagon,
growth hormone, luteinizing hormone & prolactin.
• Altered temperature regulation -- reduced basal metabolic rate --
hypothermia.
 NEUROLOGICAL
• Azotemia -- uremic encephalopathy-- Asterixis, lethargy, confusion,
seizures, and coma
• Autonomic neuropathy -- decreased baroreceptor sensitivity--
sympathetic overactivity and parasympathetic dysfunction.
Caused by Uraemia, type 2 diabetes mellitus and hyperparathyroidism
• Peripheral neuropathies -distal “glove and stocking” sensory loss
leading to motor involvement.
• Uremia- metabolite of creatinine – proconvulsant -inhibit GABA and
stimulate NMDA receptors -- increasing calcium influx into neurons --
increasing cortical activity– Seizures
What are the Anesthetic considerations ?
• AGE GROUP :
Old age
Less reserves
Difficult IV access
Difficult airway
• COMORBID:
HTN control and compliance
End organ damage
CKD

• Hb 8 – 10 mg/dL
• Preoperative rehydration – correct fluid deficit before surgery
• Target MAP > 80 mmHg
• Venous access and fistulae
Avoid cannulation and NIBP in this arm.
Protect the fistula arm with padding
• Patient weight pre and post dialysis
• Immunocompromised
• UOP monitoring >0.5mL/kg/h
• Stop nephrotoxic drugs
Concerns regarding colorectal carcinoma
• Multimodal analgesia
• Metastasis
• Risk of regurgitation
• goal-directed approach to fluid management.
• Arrange Blood & blood products --- vascualarity
Blood group , X match
 Concerns regarding GA
• Reflux – risk of aspiration
• Large fluid shifts
• Altered drug handling
What is your plan for Anesthesia?
We will opt for General Anesthesia with Endotracheal intubation with
Rapis Sequence Induction using polypharmacy and will give drugs in
titrated doses and blunting the stress response to laryngoscopy
How will you prepare this patient in
preoperative room?
 PRE MEDICATION
• Anxiolysis :
0.1 mg/kg midazolam IV preferably given
(reduced doses of Benzodiazipine)
• Preop antihypertensives: continue
• Inj Metoclopromide 5mg IV
Preanesthetic check list before Induction
• Id of patient
• Height
• weight
• Informed Consent
• Anesthesia Machine check
• Emergency drugs available and prepared.
• Difficult airway trolley.
• ER Drugs trolley.
• Defibrillator functioning.
• Art line in LA
• Attach monitors
• Cathetrize the patient
• Monitoring standard ASA 1 & 2 & invasive monitoring
How will you do induction in this patient?
 INDUCTION
• Pre oxygenate
• ATTENUATION OF STRESS RESPONSE :
• lidocaine 1.5 mg /kg IV 2 min before intubation
• Inj Dexmeditomidine 20ug IV stat 2min before intubation
• Inj Propofol 40 mg IV stat ( titrated induction according to BP)
• Inj nalbuphine 2 mg IV stat
• Inj sux 1.5 mg/kg IV stat
• Apply xylocaine gel to the tube
• Laryngoscopy and intubation
Reduce dose of induction agents to 30%
If patient does not have autonomic
dysfuntion
• PreOxygenate
• Inj Xylocaine 1.5 mg/kg 2 min before intubation
• Inj Labetalol 2-5 mg IV stat
• Inj Propofol 2 mg/kg IV stat
• Inj nalbin 4mg IV stat
• Inj Sux 1.5 mg/kg iv stat
• intubation
Ideal condition
• Inj xylocaine 1.5 mg/kg IV stat 2 min before intubation
• Inj Alfentanil 10-20ug/kg iv stat
• Inj propofol 2mg /kg iv stat
• other options : etomidate 0.2 to 0.4 mg/kg
• Inj esmolol 0.3-1.5 ug/kg iv stat 1 min before intubation
• Inj Sux 1.5 mg /kg iv stat
• Laryngoscopy
• intubate
 MUSCLE RELAXANT
• NMB of choice: Atracurium
• Succinylcholine 1.5 mg/kg (in the absence of hyperkalemia).
• Rocuronium (1 mg/kg) excreted in 24 h … single dose
• vecuronium (0.1 mg/kg) as a single dose
• cisatracurium (0.15 mg/kg)… half life is increased by 4.2 min
 INHALATIONAL AGENTS
• ISOFLURANE
• SEVOFLURANE
produce inorganic fluoride ions with prolonged use (avoid >4 MAC
hours total)
OTHER
Desflurane
 ANALGESIA
• Nalbuphine 0.1mg /kg IV is given
• Paracetamol 15mg/kg IV given
Other options
• Alfentanil and remifentanil --normal doses.
• Morphine -- morphine-6-glucuronide– potent – reduce dose.
• Avoid pethidine (meperidine)-- metabolite nor pethidine --
convulsant.
• Fentanyl –inactive metabolites
• Codeine and dihydro codeine -- prolonged half life five times-- avoid.
• Oxycodone -- active metabolites -- reduce the dose and increase the
dose interval.
• Tramadol -- O-Demethyl tramadol– eliptogenic -- avoid
Why NSAIDS are contra-indicated?
• COX1 & COX2 inhibitor-- hyperkalemia,hyponatremia and exacerbate
hypertension
• cause bleeding – prevent adhesion , aggregation &activation pf
platelets -- platelet dysfunction.
• inhibit renal prostaglandins PGE2 and PGI2 – inhibit auto regulation
 PHARMACOKINETICS
• Absorption of drugs may be affected – delayed gastric emptying.
• Distribution: The volume of distribution may be increased or decreased
depending on the total body water, protein binding of drugs, time since
last dialysis.
• Protein binding: – Protein binding of acidic drugs is decreased leading to
increased concentration of active or free fraction of the drugs bound to
albumin. (e.g. salicylates, oral anticoagulants).
• CRF leading to hypoalbuminemia secondary to proteinuria –
• uric acid and lactic acid compete with the protein binding site on
albumin – Alpha1 acid glycoprotein is bound to basic drugs (e.g. opioid
analgesics local anesthetics) and the levels are increased in CRF thereby
decreasing the unbound drug concentration
• Elimination: Drugs eliminated by the kidneys will have prolonged
elimination half lives, e.g. vecuronium.
 VENTILATION
• CONTROLED VENTILATION
• Inadequate spontaneous ventilation with progressive hypercarbia
under anesthesia can result in respiratory acidosis- exacerbate
preexisting academia -
• respiratory alkalosis-shifts the hemoglobin dissociation curve to the
left, can exacerbate preexisting hypocalcemia, and may reduce
cerebral blood flow.
INTRA OP CONCERNS
• Avoid the factors that decrease RBF
• Avoid hypotension
• Avoid hypovolemia
• Avoid hypoxemia
• Avoid nephrotoxic drugs
• Avoid sympathetic stimulation
• Avoid acidosis
FACTORS EFFECTING RENAL BLOOD
FLOW
FLUID LOSES Decreased cardiac Systemic Afferent arteriolar Renal arterial
output vasodilation vasoconstriction disease
Renal losses Heart failure Sepsis hypercalcemia Renal arterial
diuretics, polyuria stenosis
GI losses vomiting, Pulmonary embolus anaphylaxis Drugs NSAIDs, atherosclerotic,
diarrhoea amphotericin B,
ephedrine,
metaraminol,
radiocontrast agents
Cutaneous losses Acute Myocardial Anesthetic agent Hepatorenal fibromuscular
burns, Stevens- infarction syndrome dysplasia
Johnson syndrom
Haemorrhage Cardiac vulvular Drug overdose Embolic disease
disease thrombus septic
cholesterol
Abdominal
compartment
syndrome
 FLUID
• Maintain normovolemia & RPP
• Target MAP 80mmHg
• isotonic crystalloids, colloids, or both may be used
• Balanced Crystalloids salt solution
Plasma-Lyte or lactated Ringer’s solutionchloride-rich crystalloids
• BLOOD LOSS:
Replace with packed red blood cells or colloid
• Albumin solutions can be indicated in renal patients with high fluid
demands to lessen interstitial volume overload
 EXTUBATION
• Extubation plan depend on how surgery went.
• If extubation planned--fully awake extubation
• Blunt stress response at extubation.
• Check ABGs.
• Should be done in upright position.
• After complete resolution of neuromuscular blockade (evidenced by
neuromuscular stimulator, return of airway reflexes, sustained head lift for
>5sec and generation of adequate tidal vol).
• neostigmine(0.04-0.08mg/kg) + gylcopyrrolate(0.2mg) IV
• Prolonged excretion
• Emergency airway equipment should be available in case re- intubation is
required.
POST OPERATIVE CARE
• Targeted fluid ( drain ,uop ,hemodynamics) inf R/L 100ml /h IV
• Pain Management– Multimodal Analgesia
• Antibiotic dose adjustments
• DVT prophylaxis
• Supplemental Oxygen: prolonged sedative effect of opioids
• Post-op renal function tests
• Coordinate with Renal unit regarding need of dialysis
• Avoid nephrotoxic drugs
• Shift patient to HDU
 ANALGESIA
• DRUGS
Lidocaine infusion
Dexmeditomidine
Paracetamol
Opioids

• PCA
• Peripheral Nerve blocks
• Thoraxic epidural
• Preoperatively at T9-T10
• Classical TAP block
• Bilateral quadratus lumborum block
• Bilateral erector spinae plane
• Rectus sheath block
• Paravertebral block
• THANK YOU