The

 Only  Basic  Surgery  

Note    
You  Need  
 
 
Prepared  By:    
Dr.  Samuel  Getahun  
Dr.  Seyfe  Bekele  
Dr.  Solomon  Bekele  
Dr.  Dawit  G/Giorgis  
Dr.  Abay  Gosaye  
 
 
 
Oct.,  2017  
 
 
 
 
  

 
 
1.   Outline  the  different  types  of  shock  and  discuss  homeostatic  
mechanisms  of     hypovolemic  shock.  
 
ANSWER  
       
•   Shock  is  a  state  of  tissue  hypoperfusion  marked  by  impaired  delivery  
of  substrates  and  removal  of  metabolic  waste.  
•   Types:  
a)   Hypovolemic  
b)   Septic/  vasogenic  
c)   Cardiogenic  
d)   Neurogenic  
e)   Traumatic  
f)   Obstructive  

Pathophysiology  of  shock:  

•   Regardless  of  etiology,  the  initial  physiologic  responses  in  shock  are  driven  by  tissue  
hypoperfusion  and  the  developing  cellular  energy  deficit.  

•   The  specific  responses  will  differ  based  on  the  etiology  of  shock.    

•   The  pathophysiologic  responses  vary  with  time  and  in  response  to  resuscitation.    

•   compensated  phase  

•   decompensation  phase  

•   Irreversible  phase    

•   Responses  

NEUROENDOCRINE    RESPONSE    

v  GOAL:    to  maintain  perfusion  to  the  heart  and  the  brain.  
Ø   STIMULI  
 
 
 a.   loss  of  circulating  blood  volume  
b.   pain,  hypoxemia,  hypercarbia,  acidosis,  infection,  change  in  temperature,  
emotional  arousal,  or  hypoglycaemia.  
Ø   Afferent  Signals  
v   Baroreceptors  
v   Chemoreceptors  in  the  aorta  and  carotid  bodies    
v   a  variety  of  protein  and  nonprotein  mediators  
v   Pain  receptors    
 
a.   Baroreceptors:  found  in  atria  ,aortic  arches  and  carotid  
bodies.  
•   They  sense  change  in  circulatory  volume  or  pressure.  
•   Their  activation  leads  to  decreased  inhibitory  output  to  the  
ANS.  

Activations  of  ANS  will  lead  to:  

Ø   Inc.  HR  and  contractility  by  β1  activation  àInc.  workload    

•   Arteriolar  vasoconstriction  by  α1  activation  leading  to      
increased    SVR  and  BP    
•   Constriction  of  venous  vessels  decreasing  venous  
Capacitance  and  Increasing  blood  return  to  the  central  
circulation.    
•   increases  catecholamine  release  from  the  Adrenal  gland  
which  increases  hepatic  gluconeogenesis  and  glycogenolysis,  
decreases  insulin  production  and  increases  glucagon  
production,  these  will  lead  to  hyperglycemia  ,  lipolysis  and  
proteolysis  
 
b.   Chemoreceptors  :  found  in  aorta  and  carotid  bodies  
•   sensitive  to  changes  in  O2tension,  H+  ion  concentration,  
and  carbon  dioxide  (CO2)  levels.    

 
 
 •   Stimulation  results  in  vasodilation  of  the  coronary  arteries,  
slowing  of  the  heart  rate,  and  vasoconstriction  of  the  
splanchnic  and  skeletal  circulation  

•    

3.   Pain  

The  sensation  of  pain  from  injured  tissue  is  transmitted  via  the  spinothalamic  tracts,  resulting  in  
activation  of  the  hypothalamic-­‐pituitary-­‐adrenal  axis,  as  well  as  activation  of  the  autonomic  
nervous  system  (ANS)  to  induce  direct  sympathetic  stimulation  of  the  adrenal  medulla  to  release  
catecholamines.  

Peculiarities  to  specific  types  of  shock  

o   SVR  is  decreased  in  neurogenic  and  septic  shock.  
o   Venous  capacitance  is  increased  in  septic  shock.  
o   CVP  is  increased  in  cardiogenic  shock.  

HORMONAL  RESPONSE(HPA  AXIS)  

v  There  will  be  release  of  cortisol,  ADH  and  Renin  in  response  to  
intravascular  volume  change  and  pain.  
v  Hypothalamic-­‐pituitary-­‐adrenal  axis  will  be  activated.  
o   CRHàACTHàCORTISOLàcatabolic  state  
o   Effects  of  Cortisol    
§   increased  hepatic  gluconeogenesis    
§   insulin  resistance,    
§   proteolysis  ,  
§    lipolysis,  and    
§   promote  water  and  sodium  retention  by  the  tubules.                                                    

 
 
 v  ADH  release  will  be  stimulated  by  hypovolemia  increased  plasma  
osmolality,  Epinephrine,  angiotensin  II,  pain,  and  hyperglycaemia.    
Its  effects  are  
o   increase  water  permeability,  decrease  water  and  sodium  losses  in    distal  tubule  
and  collecting  duct  of  the  nephron,    
o    preserves  intravascular  volume.    
o   potent  mesenteric  vasoconstrictor,  shunting  circulating  blood  away  from  the  
splanchnic  organs  during  hypovolemia.  
o   Increases  hepatic  gluconeogenesis  and  increases  hepatic  glycolysis.  
 
v   RAAS  will  be  stimulated  by  Decreased  renal  artery  perfusion,  β-­‐
adrenergic  stimulation,  and  increased  renal  tubular  sodium  concentration.  
o   Angiotensin  II  is  a  potent  vasoconstrictor  of  both  splanchnic  and  
peripheral  vascular  beds  and  stimulates  the  secretion  of  aldosterone,  
ACTH,  and  antidiuretic  hormone  (ADH).  
o   Aldosterone  promotes  reabsorption  of  sodium  and  water.  Potassium  
and  hydrogen  ions  are  lost  in  the  urine  in  exchange  for  sodium.  
 

METABOLIC  RESPONSES  
o   In  a  state  of    dysoxia  there  will  be  shift  to  anaerobic  metabolism  with  
resultant  depletion  of  ATP  and  lactate  production  leading  to  intracellular  
metabolic  acidosis  which  might  lead  to  irreversible  cell  injury  and  death    
o    The  depletion  of  ATP  potentially  influences  all  ATP-­‐dependent  cellular  
processes.  

IMMUNE  AND  INFLAMMATORY  RESPONSE          

o   Can  be  an  etiology  (like  in  traumatic  and  septic  shock)  or  effect  of  shock.  
o   The  release  of  intracellular  products  from  damaged  and  injured  cells  can  
have  paracrine  and  endocrine-­‐like  effects  on  distant  tissues  to  activate  the  
inflammatory  and  immune  responses  

 
 
 o   These  molecules  that  are  released  from  cells  are  known  as  damage-­‐
associated  molecular  patterns  (DAMPs)  
o   DAMPs  are  recognized  by  cell  surface  receptors  to  effect  intracellular  
signaling  that  primes  and  amplifies  the  immune  response.  This  leads  to  
secretion  of  proinflammmatory  cytokines  (IL1,  IL6,  IL8,  TNF,  IF)  

o   These  receptors  are  known  as  pattern  recognition  receptors  (PRRs)  and  
include  the  Toll-­‐like  receptors  (TLRs)  and  the  receptor  for  advanced  glycation  
end  products.    
 
 
2.   Define  septic  shock  in  terms  of  observable  clinical  and  laboratory  
parameters.  
o   Septic  shock  is  Sepsis  with  hypotension  (arterial  blood  pressure  <90  mmHg  
systolic,  or  40  mmHg  less  than  patient's  normal  blood  pressure)  for  at  least  1  
hr  despite  adequate  fluid  resuscitation;  
                                                                       or    
o    Need  for  vasopressors  to  maintain  systolic  blood  pressure  90  mmHg  or  mean  
arterial  pressure  70  mmHg  
 
ANSWER:  
Clinical   Laboratory  

HR>100   WBC=<4000/>12000  

RR>20   Lacticacidosis  

T>38  OR  <36   Increased  creatine  

BP<90   Blood  culture  

Focus  of  infection   Deranged  Billirubin  

 
 
 Altered  consciosness   Decreased  platelet  count  

Unresponsive  to  fluid   Base  Deficit  

Decreased  urine  output    

 
 
3.  Physiologic  and  biochemical  change  in  hypovolemic  shock.  
Biochemical  changes:-­‐  Hyperglycemia  
•   Increased  gluconeogenesis  
•   Increased  glycogenolysis  
•   Increased  proteolysis  
•   Increased  lipolysis  
•   Increased  K  &  H  loss  
•   Increased  retention  of  H2o  
4.  ECF  change  in  hypovolemic  shock.  
ANS  ;  
 Hypovolemic  shock  is  due  to  loss  of  circulatory  volume  due  to  loss  
of  whole  blood,  plasma,  interstitial  fluid  or  a  combination  of  these.  
As  we  can  see  the  loss  is  primarily  from  the  
ECF…………………………………………………………………………………………………
………………………………………………………………………………………………………
………………………………………………………………………………………………………
……………………………………………………    
5.   Indicate  in  what  clinical  findings  it  is  possible  to  assess  the  degree  of  
hypovolemic  shock  due  to  bleeding.  

 
 
  
 
 
Hemorrhagic shock can be categorized into three grades of severity based on the magnitude of
blood loss: compensated shock, uncompensated shock, and lethal exsanguination.

Compensated shock syndrome occurs if the blood loss is less than 20% of the blood volume.
Patients in compensated shock maintain adequate perfusion of the brain and heart and normal
mean arterial pressure because vasoconstriction mediated by neuroendocrine reflexes decreases
blood flow to the skin and skeletal muscle. With mild to moderate compensated shock patients
can readily survive if they drink liquids. Those in compensated shock who cannot drink water
can shift fluid within their ECF compartment. Patients with less than a 20% deficit in blood
volume over a period of a few hours can adjust the flow of fluid through the interstitial-
lymphatic compartment and achieve net transfer of fluid from the interstitium to the plasma
compartment.

Patients with uncompensated shock syndrome are hypotensive after acute hemorrhage in which
losses are equivalent to 20% to 40% of their blood volume. This magnitude of blood loss in a 70-
kg man corresponds to the loss of 1 to 2 L from an estimated blood volume of 5 to 6 L. Patients
in uncompensated shock cannot sustain mean aortic pressure by vasoconstriction, have low
cardiac output, are subject to anaerobic stress, and have acidemia that is proportional to the
severity of their shock insult. Patients in uncompensated shock for hours are at risk for death.

Those threatened by exsanguinating hemorrhage rapidly lose more than 40% of their blood
volume and profound hypotension develops. With severely reduced blood flow to their brain,
these patients become comatose within minutes and die of cardiac arrest.

 
6.  classify  shock  and  indicate  the  common  feature  in  all                                
                         types  of  shock.  
Several  features  of  shock  are  common  among  all  types  of  shock  
(cardinal  findings),  while  other  features  may  suggest  a  particular  type  

 
 
 of  shock  (suggestive  findings).  Cardinal  features  include  hypotension,  
oliguria,  cool  and  clammy  skin,  abnormal  mental  status,  and  
metabolic  acidosis  
.……………………………………………………………………………………………………………
……………………………………………………………………………………………………………
………………………………………………….  
 
 
 
7.  GIVE  a  brief  outline  of  the  pathogenesis  of  septic  shock.  
 
ANSWER  
•   is  the  result  of  dysfunction  of  the  endothelium  and  
vasculature  secondary  to  circulating  inflammatory  mediators  
and  cells.    It  occurs  as  a  result  of  exaggerated  inflammatory    
response  of  the  body  to  an  infectious  insult.  
•   Gram-­‐positive  and  gram-­‐negative  bacteria  and  fungi  have  
unique  cell  wall  molecules  called  pathogen-­‐associated  
molecular  patterns  (PAMP)  that  bind  to  pattern  recognition  
receptors  (called  toll-­‐like  receptors  [TLRs])  on  the  surface  of  
immune  cells.  
•   In  the  attempt  to  eradicate  the  pathogens,  the  immune  and  
other  cell  types  (e.g.,  endothelial  cells)  elaborate  soluble  
mediators  (proinflammatory  mediators  IL-­‐1,IL-­‐6,TNF)    that    
o   enhance  macrophage  and  neutrophil  killing  effector  
mechanisms,    
§   The  Neutrophils  and  Endothelial  cells  produce  and  
activate:  
o   iNO-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐-­‐àVasodilatation  
o   Arachidonic  acid  metabolites-­‐à  vasodilatation  
o   O2  radicals-­‐-­‐-­‐à  tissue  destruction  

 
 
 o   Coagulation  cascade-­‐à  microthrombosis-­‐à  
Ischemia  
o   Bradykinin  -­‐-­‐àcapillary  leak  
 
These  will  lead  to  organ  injury.  
 
o   increase  procoagulant  activity  and  fibroblast  activity  to  
localize  the  invaders,  and    
o   increase  microvascular  blood  flow  to  enhance  delivery  of  
killing  forces  to  the  area  of  invasion.  
•   When  this  response  is  overly  exuberant  or  becomes  systemic  
rather  than  localized,  manifestations  of  sepsis  may  be  
evident.  
o   These  findings  include  enhanced  cardiac  output,  
peripheral  vasodilation,  fever,  leukocytosis,  
hyperglycemia,  and  tachycardia  
                     
 
 
 
 
8.   Hypovolemic  shock  management  
 
o    Airway  
o   Breathing  
o   Circulation  
o   Secure  large  bore  bilateral  IV  lines  and  send  blood  for  CBC  
and  blood  group  
o   Start  crystalloids  30ml/kg  to  run  as  fast  as  possible  
§   Reassess  with  clinical  parameters  
•   Pulse    
•   Blood  pressure  
•   Urine  output  
 
 
 •   Mentation    
§   Catheterize  and  monitor  UOP  
§   Control  of  On-­‐going  Hemorrhage    

–   direct  pressure,  surgical  control,  immobilization  of  

#,  or  tourniquet.    
•   Blood  transfusion  for  (Class  III  and  IV  shock)  
o   Acute  blood  loss  with  declining  Hgb  
o   >30%  estimated  blood  loss  with  clinical  symptoms  of  
persistent  hypovolemia  
o   >40  %  estimated  blood  loss  
•   Patients  with  hemorrhagic  shock  are  at  high  risk  of  
coagulopathy  so  they  should  be  transfused  with  PRBC,  FFP  
and  platlate  as  well  with  a  ratio  of  1:1:1  
 
•   In  cases  of  severe  and  prolonged  hypovolemia  
vasopressors  can  be  considered.  
•   Prevent  hypothermia  
o   Clothing  
o   Keep  the  room  warm  
o   Use  warm  fluids  
•   Pain  management  
•   MONITORING  
o   Blood  pressure  and  pulse;a  mean  arterial  pressure  of  
65  and  SBP  OF  110mmhg  and  HR  60-­‐100  
o   Central  venous  pressure  monitoring  
o   Urine  output  above  0.5  ml/kg  
o   Oxygen  saturation  above  94%  
o   Mental  status  should  be  assessed  frequently  
o   Serum  lactate  level  &  base  deficit  
 
 
Additional  points  for  traumatic  shock  
 
 
 •   prompt  control  of  hemorrhage  ,  
•    adequate  volume  resuscitation  ,  
•    debridement  of  nonviable  tissue  ,    
•   stabilization  of  bony  injuries  ,  and  
•    appropriate  treatment  of  soft  tissue  injuries.    
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
9.   SEPTIC  SHOCK  MANAGEMENT  
 
o   Airway  
o   Breathing:  supplemental  oxygen  
o   Circulation  
o   Secure  large  bore  bilateral  IV  lines  and  send  blood  for  CBC  
and  blood  group  
o   Start  crystalloids  30ml/kg  as  fast  as  possible  
§   Reassess  with  clinical  parameters(  PR,  BP,  SPO2,  
Temp,  Mentation,  UOP)  
§   Catheterize  and  monitor  UOP  
 
 
 o   Vasopressors  
§   Norepinephrine  is  the  first  choice  
§   Goal  :  target  a  mean  arterial  pressure  (MAP)  of  65  mm  
Hg  
o   Goals during the first 6 hrs of resuscitation:
a) Central venous pressure (CVP) 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d)  Central  venous  (superior  vena  cava)  or  mixed  venous  
oxygen  saturation  70%  or  65%,  respectively  
o   Start  empirical  Antibiotic  therapy  within  the  first  hour  after  
sending  blood  for  culture  and  sensitivity  
§   Usually  for  7-­‐10  days  
§   Revise  based  on  sensitivity  results  
o   Source  control  
o   Drainage  of  Intra-­‐abdominal  abscess,  Thoracic  empyema…  
o    Debridement  of  Necrotizing  fasciitis,  …….  
o   Device  removal:  Infected  vascular  catheter,  Urinary  catheter  
o   Definitive  control:  Cholecystectomy,    Sigmoid  resection….  
ü   Steroids    
o   If  SBP<  90mmHg  despite  appropriate  fluid  and  vasopressors  
o   Hydrocortisone  200mg  IV/day  
ü   Blood  transfusion  
o   Give  red  blood  cells  when  hemoglobin  decreases  to  7.0  g/dL  (70  
g/L).  
o   We  suggest  prophylactic  platelet  transfusion  when  counts  are  <  10,000/mm3  (10  ×  
109/L)  in  the  absence  of  apparent  bleeding  and  when  counts  are  <  20,000/mm3  (20  ×  
109/L)  if  the  patient  has  a  significant  risk  of  bleeding.  Higher  platelet  counts  (≥  
50,000/mm3  [50  ×  109/L])  are  advised  for  active  bleeding,  surgery,  or  invasive  
procedures  
 
o   Glucose  control  
o   target  an  upper  blood  glucose  level  ≤  180  mg/dL  

 
 
 o   monitored  every  1  to  2  hours  until  glucose  values  and  
insulin  infusion  rates  are  stable,  then  every  4  hours  
thereafter.  

ü  DVT prophylaxis
 
o   UFH  5000  IU  sc  BID  
o   LMWH  –  enoxaparin  40  mg  sc  daily  
o   Use  low-­‐dose  heparin,  unless  contraindicated    
o   Use  a  mechanical  prophylactic  device,  such  as        
compression  stockings  or  an  intermittent  compression  
device,  when  heparin  is  contraindicated    
o   Use  a  combination  of  pharmacologic  and  mechanical  
therapy  for  patients  who  are  at  very  high  risk  for  deep  
vein  thrombosis    
ü   Stress  ulcer  prophylaxis  
o   H2  blockers  or  PPI  
o   E.g.    cimetidine  200  mg  IV  BID  
ü   NUTRITION  
o   Initiate  early  enteral  nutrition  
Components of Damage Control or Hemostatic Resuscitation
  Components of damage control resuscitation

  Permissive hypotension until definitive surgical control

  Minimize crystalloid use

  Initial use of 5% hypertonic saline (HTS has consistently been shown to

reduce the inflammatory response and is thus considered to be
immunomodulatory)

  Early use of blood products (PRBCs, FFP, platelets, cryoprecipitates)

  Consider drugs to treat coagulopathy (rFVIIa, prothrombin concentrate,
TXA)

 
 
  
1.  Outline  the  physiologic  responses  to  trauma.  
 
Ø  Neuroendocrine    responses  
•   Stimuli  and  responses  include  
o   Pain:  stimulates  the  HPA  axis  (CRFàACTHà  cortisol)  
§   Effects  of  cortisol  
•   Gluconeogenesis  
•   Proteolysis  
•   Lipolysis  
•   Insulin  resistance  and  hyperglycemia  
•   promote  water  and  sodium  retention  by  the  tubules  
•   Immunosuppression    
o   Hemorrhage  and  hypovolemia:  baroreceptor  activation  à  loss  of  
inhibition  of  nervous  system  leading  to  
§    Central  neural  stimulation  of  ACTH,  ADH    and  GH  from  pituitary  
gland  
ACTHà  CORTISOL    and  glucocorticoids  from  adrenal  cortex    

ADH  

o   increase  water  permeability,  decrease  water  and  sodium  losses  in    distal  tubule  
and  collecting  duct  of  the  nephron,    
o    preserves  intravascular  volume.    
o   increases  hepatic  gluconeogenesis  and  increases  hepatic  glycolysis.  
§   Sympathetic  neural  activity  increases  and    there  will  be  enhanced  
secretion  of  
•   epinephrine  and  norepinephrine  from  the  adrenal  medulla,    
o   increase  CO  and  elevate  BP  

 
 
 o   Epinephrine  stimulates  glycogenolysis  and  
lipolysis  and  inhibits  release  of  insulin    
o    
•    renin  from  the  kidney  à  RAAS  activation    
o   Aldosterone  promotes  reabsorption  of  sodium  and  water.  
Potassium  and  hydrogen  ions  are  lost  in  the  urine  in  
exchange  for  sodium.  
 
•   glucagon  from  the  pancreas  
o   Increases  blood  glucose  through  stimulation  of  
glycogenolysis,  gluconeogenesis,  and  lipolysis    
o   Tissue  hypoxia  or  hypoxemia:  sensed  by  chemoreceptors  
o   Emotional  arousal  à  activation  of  ANS  
o   Infection  à  SIRS  
o   Changes  in  temperatureà    
 
•   IMMUNE  RESPONSES  
•   Proinflammatory  phase:  the  cytokines  IL1,  IL  6,  IL8  ,TNF-­‐a  
§   Directly  act  on  z  hypoyhalamusà  pyrexia  
§   Augment  hypothalamic  stress  response  
§   Cause  skeletal  mm  proteolysis  directly  
§   Induce  acute  phase  proteins  production  in  z  liver    
§   Play  role  in  peripheral  insulin  resistance  
•   Counter  regulatory  phase:    
§   IL-­‐1  receptor  antagonist  (IL-­‐1Ra)  and  TNFsoluble  
receptors  (TNF-­‐sR-­‐55  and  75)  
§   Prevent  excessive  proinflammatory  activities  
§   Restore  homeostasis  
§   If  prolonged  or  excessive,  may  evolve  into  CARS  
 
 
  
 
2.  Discuss  phases  of  physiologic  response  to  trauma.  
•   Ebb  and  flow  phases  
EBB  PHASE  
•   Begins  at  the  time  of  injury  and  lasts  for  24  to  48  hrs  
•   Predominantly  regulated  by  :  catecholamines,  cortisol  and  
aldosterone  
•   Role  :  to  conserve  both  circulating  blood  volume  and  energy  
source  for  recovery  and  repair  
•   Characterized  by  
•   Hypovolemia  
•   Dec.  BMR  
•   Dec.  CO  
•   Hypothrmia  
•   Lactic  acidosis  

FLOW  PHASE  :  subdivided  into  catabolic  and  anabolic  phases  

v  Catabolic  phase:  lasts  for  3  to  10  days  
o   Regulated  by  cytokines  and  counterregulatory  hormones  
o   Role:    Mobilisation  of  energy  stores  for  Recovery  &  Repair  
o   Characterized  by  
§   ↑  BMR,  ↑  Temp,    ↑  O2  consump,  ↑  CO    
§   Insulin  resistance  ,  Hyperglycemia  
§   Lipolysis,  prroteolysis  
§   Increased  urinary  nitrogen  excretion  
 
 
 
 v    Anabolic  phase:    
o    Lasts  for  10  to  60  days  
o   Role  :  replacement  of  lost  tissues  
o   Mediated  by—GH,  IGF,  INSULIN  
o   Characterized  by  
§   Reaccumulation  of  body  fat  and  proteins  
§   Positive  nitrogen  balance  
3.  Discuss  changes  in  body  composition  following  injury.  
 
v  Catabolism  leads  to  a  decrease  in  fat  mass  and  skeletal  
muscle  mass  
•   Liver  glycogenolysis  (16hrs)à  muscle  glycogenolysis  (24-­‐48  hrs)  
à  lipolysis  from  GI,  omentum,  heart  (7days)à  peripheral  :  
skeletal  and  intestinal  (3-­‐5days)  à  structural  and  elemental  
proteins  (heart,  kidneys)  (14-­‐21  days).  

 
 
v  Body  weight  may  paradoxically  increase  because  of  
expansion  of  extracellular  fluid  space  
…………………..  
 
4.  List  avoidable  factors  that  compound  the  response  to  
injury.  
•   Continuing  haemorrhage    
•      Hypothermia:  results in increased elaboration of adrenal ster- oids and
catecholamines.  
 
•      Tissue  oedema    
 
 
 •      Tissue  underperfusion    
•      Starvation    
•   Avoiding unnecessary fasting in the first instance and early
oral/enteral/parenteral nutrition form the platform for avoiding loss
of body mass as a result of the vary- ing degrees of starvation
observed in surgical patients.
•      Immobility    
•   Avoidance of unnecessary bed rest and active early mobilisation
are essential measures to avoid muscle wasting as a consequence
of immobility.
 
 
5.  List  strategies  to  prevent  unnecessary  aspects  of  the  
stress  response.  
•   Minimal  access  techniques  
•   Adequate  peri-­‐op  fluid  therapy  
•   Minimal  periods  of    peri  op  Starvation    
•   Epidural  analgesia      
•   Early  mobilization  
•   Early  return  to  oral  feeding    
 

 
 
 
 
 
 
 
 
 
 
 
 
1.  Define  MODS.  
 
o   Progressive   physiologic   failure   in   two   or   more   organ  
systems   in   a   critically   ill   patient,   such   that   homeostasis  
cannot  be  maintained  without  intervention.    
 
2.  What  are  the  clinical  factors  that  predispose  a  surgical  patient  to  
MOF?  

3.  Discuss  the  Pathophysiology  of  MODS.  

•   It  is  the  culmination  of  generalized  and  excessive  
neuroendocrine,  immune  and  inflammatory  resonse  to  injury.    
•   The  Systemic  inflammatory  response  to  injury  can  be  broadly  
compartmentalized    into    
o   A  proinflammatory  Phase    

 
 
 §   activation    of  cellular  processes  designed  to  restore  
function  and  eradicate  invading  microbes  
o   An  anti-­‐inflammatory(counter  regulatory)  phase  
§   prevents  excessive    proinflammation  Activation  and    
restores  homeostasis  
Ø  when  the  proinflammatory  Response    to  an  insult      predominates  
,  SIRS  result    
                             -­‐responsible  for  early  MOF  (occurs  with  in  72hrs  of  the  
initial  insult  and  precipitated  by  cellular  shock)  
Ø    when  the  anti  –inflammatory  response  to  an  insult    
             predominates  ,CARS,  immunosuppression  ,  &    ↑sed      
             susceptibility  to  infection  ensue.  
                               -­‐responsible  for  late  MOF  (typically  6-­‐8  days  after  the  
insult  and  is  usually  related  to  infection  )  
 
4.  Discuss  theories  in  the  Pathophysiology  of  MODS.  
 
a.  MACROPHAGE  HYPOTHESIS  OF  MOF  
o   Excessive  or  prolonged  activation  of  macrophages                                            

                                                                 
o   Excessive  production,  surface  expression,  and  liberation  of  
cytokines  (TNF,  IL1,  IL6,  INF,  CSF)                      

                                                                 
o   additional  humoral  and  cellular  effector  systems                              

                                                                   
o   deleterious  local  and  systemic  effects    

 
 
 o   endothelial   cell   injury   with   tissue   factor   release,↑ed  
permeability,&  edema  formation    
o   systemic  effects  include  hemodynamic  instability,  acute  
lung  injury  &  widespread  organ  damage.  
b.  MICROCIRCULATORY  HYPOTHESIS  OF  MOF  
o   Regardless   of   the   cause,   inadequate   oxygen   availability  
rapidly  leads  to  cellular  dysfunction,  injury,  and  ultimately  
cell  death,  with  the  net  result  being  organ  dysfunction.  The  
re-­‐establishment   of   blood   flow   after   ischemia   can   itself  
cause  tissue  injury.    
c.  GUT  HYPOTHESIS  OF  MOF  
o   Intestinally  derived  bacteria  or  endotoxin  serve  as  triggers  
to   initiate,   perpetuate,   or   exacerbate   the   septic   state   and  
thereby   promote   the   development   of   MOF   in   patients  
without  evidence  of  infection  
o   Once  initiated  it  can  become  self-­‐sustaining.  
Ø   the   products   of   endotoxin-­‐activated  
macrophages     in   conjunction   with   endothelial   cells                    
impair   oxygen   delivery   to   the   gut  
increasing   intestinal   permeability            
translocation  of  intestinal  endotoxin.  
d.   TWO  HIT  PHENOMENON  
Ø  The   host   experiences   sequential   insults   such   that   the  
subsequent  systemic  inflammatory  response  exceeds  the  typical  
response  elicited  by  either  insult  alone.  
Ø    The   initial   insult   primes   the   inflammatory   response,   and  
patients  enter  a  state  of  systemic  hyperinflammation  (i.e.,  SIRS).  

 
 
 Ø    If   the   insult   or   the   inflammatory   response   is   exaggerated   or  
perpetuated,   patients   enter   a   state   of   malignant   systemic  
hyperinflammation   (severe   SIRS)   that   can   evolve   into   overt  
MOF,  independent  of  other  factors.    
Ø    A   second   insult   during   a   vulnerable   period   amplifies   SIRS   to  
produce  MOF.    
5.  Discuss  specific  organ  dysfunctions  in  MODS  
a.  Respiratory  dysfunction    
Ø  ARDS  (Shock  lung)  
•  Acute  hypoxemic  resp.  failure    following  a  systemic  or  pulmonary      
insults  w/o  evidence  of  heart  failure.    
•  PaO2/   FIO2   ratio   lower   than   200   mm   Hg   in   association   with  
bilateral   fluffy   pulmonary   infiltrates   and   a   pulmonary   capillary  
wedge  pressure  lower  than  18  mm  Hg.H20.    

 
 
6.  Outline  principles  of  management  of  MODS  
•   See  mgt  of  septic  shock    
                                   +  
•   Supportive  mgt  for  specific  organs  
o   ARDS-­‐-­‐-­‐  mechanical  ventilation  
o   Hemodialysis  
7.  List  prognostic  indicators  of  MODS  
 
a.   Number  of  failing  organs  
b.  Underlying  illness  
c.   Duration  of  organ  dysfunction  
d.  Advanced  age  
e.   Premorbid  illness    
 
 
 
 
1.   Mention   reasons   that   explains   why   fluid-­‐electrolyte   and   pH  
changes  are  a  more  serious  problem  in  children  than  what  they  
are  in  adults.  
 
o   Infants  have  higher  metabolic  rate  than  adults  
o   Infants  have  greater    proportion  of  body  water  to  weight    
o   Much  of  TBW  is  in  ECF  –prone  to  fluid  overload  and  loss,  narrrow  
margin.  
o   Infants   have   a   greater   proportion   body   surface   area   to   weight    
-­‐↑  evaporative  loss    
o   Infants   have   limited   ability   to   dilute   and   concentrate   urine-­‐
immature  kidney.  
o   Infants  are  dependent  on  others  to  meet  their  fluid  needs  
 
2.   Discuss  phases  of  fluid  balance  in  infants.  
o   Pre-­‐diuretic  phase  
o   Up  to  1st  24hr  
o   Low  OUP    (<  1ml/kg/day)  
o   GFR  is  low  
o   Causes    
§   Low  RBF  (6%  of  CO    Vs.  25%  in  adult)  
§   High  reno-­‐vascular  resistance  
§   Starts  to  decrease  after  1st    day  post  natal  period  
o   Excess  fluid  administration  will  lead  to  fluid  over  load  
o   Diuretic  phase    
o   2nd  day-­‐72hr  
o   High  UOP  (Up  to  7cc/kg/day)  
o   High  Na  and  water  loss  may  be  encountered  

 
 
 §   Dramatic   shifts   in   fluid   from   the   intracellular   to  
extracellular   compartment   result   in   a   diuresis   and  
natriuresis  
o   Neonate  who  do  not  achieve  –ve  fluid  balance  during  this  
phase   are   at   an   increased   risk   of   PDA,   CHF,   and   chronic  
lung  disease    
o   Term  infants  are  able  to  conserve  sodium,  but  premature  
infants  are  considered  “salt  wasters”.  
o   Post-­‐diuretic  phase    
o   Start  from  day  4  –  5  
o   UOP   and   Na   excretion   begin   to   vary   based   on   fluid   and  
electrolyte  administration/ingestion  
o   GFR  increased  rapidly  in  proportion  of  body  weight  
o   Slowly  increase  to  reach  adult  level  at    1  to  2  yrs.  

3.   Compartments  of  body  fluids.  

 
™   Intracellular  water:  2/3  of  TBW  
™   Extracellular  water:  1/3  TBW  
-­‐    Plasma:  1/3  of  extracellular  water  
-   Interstitial  space:  2/3  of  extracellular  water  
 
4.   Describe   the   principles   of   fluid   and   electrolyte   therapy   in  
pediatric  patients.  
 
This  is  divided  into  3  phases.  
1)  Deficit  therapy  -­‐  management  of  fluid  and  electrolyte  losses  that  occur  
prior  to  presentation.  

 
 
2)  Maintenance  therapy  -­‐  replace  loss  under  ordinary    condition    
3)  Replacement  therapy  -­‐  Replace  ongoing  abnormal  loss  
 
5.   Pathophysiology  and  mgt  of  fluid  and  electrolyte  imbalance  in  
a  child  with  IHPS.  
 
The     primary   metabolic   disorder   is   :   hypkalemic,   hypochloremic,  
metabolic  alkalosis  with  paradoxic  aciduria.  
Physiologic  correction  
o   At  cellular  level  by  Na+  -­‐  K+  ATPase:  Na  shifts  out  of  cells  and  K+  
enters  into  cells.  This  corrects  for  the  first  3  days.  
o   RAAS   will   be   activated   by   hypovolemia   and   hyponatremiaà  
conservation  of  Na  and  loss  of  K+  and  H+  at  distal  and  collecting  
tubulesàparadoxic   aciduria   with   hypokalemia   and  
hypochloremia.  

The  vomiting  of  hydrochloric  acid  results  in  hypochloraemic  alkalosis  

but,  initially,  sodium  and  potassium  levels  may  be  relatively  normal.  
However,  as  dehydration  progresses,  more  profound  metabolic  
abnormalities  arise,partly  related  to  renal  dysfunction.  Initially,  the  
urine  has  a  low  chloride  and  high  bicarbonate  content,  reflecting  the  
primary  metabolic  abnormality.  This  bicarbonate  is  excreted  along  with  
sodium  and  so,  with  time,  the  patient  becomes  progressively  
hyponatraemic  and  more  profoundly  dehydrated.  Because  of  the  
dehydration,  a  phase  of  sodium  retention  follows  and  potassium  and  
hydrogen  are  excreted  in  preference.  This  results  in  the  urine  becoming  
paradoxically  acidic  and  hypokalaemia  ensues.  
 
 
6.   Perioperative  fluid  and  electrolyte  mgt  of  a  pediatric  pt.  
Principle  
 
 
  
Fluid  deficit  (L)  =  PIW  (kg)  –  IW  (kg)  

 
Nadeficit  =  (Nadesired  –  Nacurrent)  x  (0.6)  x  (Body  wt.  in  Kg)  
K  deficit  =  (K  desired  –  K  current)  X  0.4  X  body  wt  in  kg  replace  in  8  hrs  
Intra  op  :        MF  +  preoperative  FD  +  3rd  space    losses  +    EBL  

           Post  op  :        MF  +  preoperative  or  intraoperative  FD  +  OL  

 
 
•   e.g.  4  -­‐month-­‐old  infant  presents  numerous  watery  diarrhea,  and  decreased  
activity.  The  weight  was  6  kg.  Weight  at  the  time  o  f  her  immunization  7  days  
ago  was  6  .6  kg.  blood  pressure  74/43  mmHg,  Sodium  124  mEq/L,  k+  =  2.5  
others  N  range.  He  is  kept  NPO  for  9hrs.  EBL=50ml.  calculate   the   pre-­‐op,  
intraop  and  post  op  fluid  mgt  for  this  pt.  
 

ANSWER  

Pre  op  

•   Deficit  :  0.6kg=  600ml  ,  MF=  600  ml  

•   Na+  deficit  (140  –  124  *  .6*  6)  =  57.6meq,  maintainance  Na+  =3meq/100ml  =18  meq  
ü   57.6  +  18  =  75.6  meq    
•   K+  deficit  :(  3.5-­‐2.5)  *0.4  *  6  =2.4meq,  maintenance  =  2meq/100  ml=12meq  
ü   12+2.4=14.4  meq  

 
 
 •   phase1   :   20ml/kg=   120   ml   bolus   –   remaining   deficit   =   480ml,   remaining   Na+   deficit=  
75.6-­‐18.4=57.2meq  
•   phase  2:    240  ml  +  1/3*600=  440  ml  for  8hrs.  +  ½  Na    
•   phase3:  240ml  +  2/3*600=  640  ml  over  16hrs.+  ½  Na  
•   Fluid  choice  :    0.45  %  NS  +  5%dextrose  +  20meq  kcl/L  
 
 
 
INTRA  OP  
MF  +  preoperative  FD  +  3rd  space    losses  +    EBL  
ü   Deficit  -­‐  Period  of  starvation  prior  to  anaesthesia    
ü   Deficit  =  normal  maintenance  fluid  rate  x  number  of  hours  starved    
ü   In  the  first  hour  of  surgery  50  %  of  the  deficit  should  be  replaced,  and  25  %  during  each  
of  the  second  and  third  hours.  
•   Redistribution  and  Evaporative  Surgical  Fluid  Losses    
ü    Minimal  (inguinal  hernia  repair)  
–   1-­‐2  ml/kg/hr  replacement    
ü   Moderate  (gallbladder  removal)  
–   2-­‐4  ml/kg/hr  
ü   Severe  (bowel  resection,  open  abdominal  surgery)  
–   4-­‐8  ml/kg/hr,  
POST  OP  
•   MF  +  preoperative  or  intraoperative  FD  +  OL  
 
7.   Maintenance  fluid  and  electrolyte  calculations  in  children.  
 
FLUID  REQUIREMENTS  (>4  weeks  old)  
a.   For  first  10  kg  100  ml/kg/day  (4ml/kg/hr)  
b.   For  second  10  kg  50  ml/kg/day  (2ml/kg/hr)  
c.   Each  additional  kg  20  ml/kg/day  (1ml/kg/hr)  
ElECTROLYTE  REQUIREMENTS  
d.   Na+  3  meq/100ml  
e.   Cl-­‐  4  meq/100ml  
f.   K+  2  meq/100ml  

             DEXTROSE  

 
 
 o   Maintenance  fluids  usually  contain  5%  dextrose  (D5),  5  g  of  carbohydrate  per  100  mL  of  
solution  or  50  g/L  which  provides  20calories/100  mL  and  nearly  20%  of  the  daily  caloric  
needs.    (or  2-­‐5gm/kg/day)  

FLUID  CHOICE  

o   Age  <  5yr:  1/3NS,  2/3  10%DW  

o   Ade  5-­‐8  yr:  ½  NS,  ½  10%  DW  
o   Age  >8  yr:  like  an  adult  

For  children  who  are  febrile  or  on  radiant  warmer:  MF  should  1.5X  normal  

 
e.g.  calculation  for  maintenance  fluid  requirements  for  a  15  kg  child  
and  fluid  of  choice.  
•   Calories:  100  calories/kg  for  1st  10  kg  +  50  calories/kg  for  5  kg  (15–
10  kg)=1250  calories/day.  
•   Water:   100   mL/kg   for   1st   10   kg   +   50   mL/kg   for   5   kg   (15–10  
kg)=1250ml/d,  rate  of  50ml/hr.  
•   Sodium:  3  mEq/100  mL  water=3mEq  ×  12.5=  36.5  mEq/day  or  30  
mEq/L  of  solution.  
•   Potassium:  2  mEq/  100  mL  water  =  2mEq  ×  12.5  =  25  mEq/day  or  
20  mEq/L  of  solution  
•   The   child   requires   intravenous   fluids   ∼   1250   mL/day,30meq/L  
NaCl,20meq/l  of  KCl.  
•   Fluid  of  choice  =5%  dextrose  with  ¼  NS  +20meq  KCL/L    
8.   Components  and  osmolarity  of  IV  fluids.  

 
 
  
R/L  also  has  27meq  of  HCO3.  
 
9.   62   y/o   male,   80   kg,   for   hemicolectomy   NPO   after   22:00,  
surgery  at    08:00,  received  bowel  prep  3  hr.  procedure,  500  
cc   blood   [Link]   are   his   estimated   intraoperative   fluid  
requirements?  
 

 
 
 
 
 

 
 
1.   What  changes  takes  place  in  stored  blood  at  4  degree  
celicius  in  two  weeks  time?(lesion  of  storage)  
 
o   Depletion  of  ATP  
o   Depletion  2,  3  BPG    
o   sodium  entry  into  RBCS    
o   Potassium  Leaks  out  of  RBCS    
o   Decrease  pH  (lactate  ,ammonium,  hydrogen)    
o   Release  of  cytokines,  bioreactive  substances  
o   Release  of  free  hemoglobin  
o   Loss  of  labile  factors  (  V  ,VIII,XI)  
o   Decreased  viability  of  platelets      

2.   Discuss  &  outline  the  list  of  components  of  blood  

transfusions  and  their  indications.  
 
a.   WHOLE  BLOOD  :    INDICATIONS  
o   Massive  hemorrhage  following  trauma  
o   Exchange  transfusion  in  neonate  
b.  PACKED  RBC  :  INDICATIONS  
o   Anemia    with  Hgb<7mg/dl  
o   Hgb  7-­‐10mg/dl  with  sign  and  symptom  of  anemia  
o   Hgb  >10  in  patient  with  acute  MI  or  unstable  angina  
c.   LEUKOCYTE  REDUCED/WASHED  RBC  
d.  GRANULOCYTE  CONCENTRATE  
e.   FRESH  FROZEN  PLASMA:  INDICATIONS  
o   Multiple  or  specific  coagulation  factor  deficiency  with  
abnormal  PT  and  or  Aptt    
o   Inherited  coagulopathies    in  which  specific  factor  
concentrate  not  available  
 
 
 o   Prior  to  invasive  and  surgical  procedures  with  high  risk  
of  bleeding  and  coagulation  test  abnormality(INR>1.5)  
o   Emergency  reversal  of  anticoagulant  therapy  
o   In  massive  hemorrhage    with  INR  >1.5  
o   Treatment  of  thrombotic  thrombocytopenic  purpura    
f.   CRYOPRECIPTATE:  INDICATIONS  
o   Hemophilia  A,  
o   Von  Willbrand  disease  and  
o    Hypofibrinogenemia    
g.   PLATELETS  :    INDICATIONS  
o   <10,000/uL(for  prophylaxis)  
o   <50,000/uL(micro  vascular  bleeding  or  planned  major  
surgery)  
o   Platelet  dysfunction    
o   <100,000/uL(for  neurosurgical  &  ophthalmologic  
procedure  
o   Active  micro  vascular  bleeding  with  thrombocytopenia  
 

3.   Discuss  briefly  the  complications  of  blood  transfusion.  

 
Ø    Immunologic  
o   Acute  hemolytic  reaction:  ABO  incompatibility  resulting  in  
intravascular  hemolysis  
§   Mgt:    
§   Stop  transfusion  and  start  saline  infusion    
§   Direct  Coombs,  plasma  free  Hgb,  BG,  crosshatch  
§   Notify  blood  bank  (switched  bags)  
 
o   Delayed  hemolytic  reaction:  
 
 
 §    Due  to  minor  RBCs  antigen  discrepancies  
§   Occur  2  to  10  days  after  transfusion  
§   Extra  vascular  hemolysis  
§   fever,  recurrent  anemia,  Jaundice.    
§   do  not  usually  require  specific  intervention(primarily  
supportive)    
 
o   Post  transfusion  purpura  
o   Anaphylaxis    
o   Urticaria    
o    Hypotension    
o   TRALI  
§   Most  common  cause  of  transfusion  related  death  
§   noncardiogenic  pulmonary  edema  related  to  
transfusion  occurring  during  or  within  six  hours  after  a  
transfusion.  
§   results  from  the  transfusion  of  donor  plasma  that  
contains  high  leukocyte  titer  anti  HLA  antibodies    that  
bind  the  recipient  leukocyte  and  ends  up  with  
interstitial  edema  &  fluid  in  alveoli.  
§   Refer  uptodate    
o   GVHD  
o   IMMUNOSUPPRESSION  
 
Ø  Non  immunologic  
o   Febrile  non-­‐haemolytic  transfusion  reactions  (FNHTRs)  
§   Most  common  complication  (1%  of  transfusion)  
§   Antibody  to  donor  WBCs  or  accumulated  cytokines  
§   Mild  -­‐  38°C,  but  <2°C  rise  from  baseline  
•   Mgt-­‐  antipyretic  ,  slow  transfusion    
 
 
 §   Moderate  -­‐  pyrexia  >2°C  above  baseline  or  >39°C  or  
rigors  ,  myalgia    
•    mgt  –  stop  transfusion,  leukocyte  reduced  blood    
o   Circulatory  Overload  
o   Bacterial  contamination  
o   Other  infections:    HBV,  HCV,  HIV,  CMV,  SYPHILLIS,  
MALARIA……..  
 
4.   Define  massive  transfusion  and  discuss  its  complications.  
 
o   It  is  transfusion  of  more  than  50  percent  of  a  patient's  blood  
volume  in  12  to  24  hrs.  or  transfusion  of  more  than  10  units  of  
blood  in  24  hrs.    
o   1:1:1  ratio  of  RBC,  platelet,  FFP-­‐  each  6units  
o   Complications:    
o   circulatory  overload  
o   Hypothermia  
o   Hypocacemia  
o   DIC  
o   Dilutional  thrombocytopenia  
o   Impaired  platelet  function  
o   Deficiency  of  factors    V,  VIII,    
o   Metabolic  alkalosis    
o   Low  2,3-­‐BPG      
o   Hyperkalemia  
o   Coagulopathy  
 
5.   Discuss  briefly  the  approach  to  a  patient  who  needs  blood  
transfusion.  

 
 
6.   Discuss  biological  phases  of  hemostasis  in  the  order  they  
occur.  
o   Hemostasis  is  the  process  of  blood  clot  formation  at  the  site  of  
vessel  injury.  
o   Phases  of  normal  hemostasis  :    
1.  Vascular  phase:  
§   period  of  arteriolar  vasoconstriction  mediated  by:  
•   Neurogenic/  myogenic  reflex  
•   Endothelin  from  endothelial  cells  
•   Thromboxane  A2  from  platelets  
2.  Platelet  phase:  PRIMARY  HEMOSTASIS  
§   platelet  plug  formation  at  sites  of  injury  which  
occurs  within    15seconds  of  injury  
§   it  stops  blood  loss  from  capillaries  ,small  arteriole  
,and      venules  
§   Three  critical  events  occur:    
•   Platelet  adhesion  and  shape  change,    
•   Platelet  secretion  (release  reaction),    
•   Platelet  aggregation  
3.    Coagulation  phase  /Secondary  hemostasis  :    
§   a  series  of  enzymatic  conversions,  turning  inactive  
proenzymes  into  activated  enzymes  and  culminating  
in  the  formation  of  thrombin.  
§   Has  2  pathways:  Extrinsic  and  Intrinsic  
•   Intrinsic:  Initiated  by  negatively  charged  
surface  
•   Extrinsic  :  Initiated  on  tissue  injury  
4.  Fibrinolytic  phase  
§   Control  of  coagulation    
 
 
 §   Antithrombins  (e.g.,  antithrombin  III)  
§   Proteins  C  and  S  
§   Fibrinolytic  cascade    

7.   Classify  and  give  examples  for  bleeding  disorders.  

 
a.   VASCULAR    ABNORMALITIES:    examples  
ü   Vit  c  deficiency  
ü   TTP  
ü   HUS  
b.  PLATELET  DISORDERS  
o   Quantitative  
1.  Examples:  HIT,  ITP….  
o   Qualitative  
1.  Examples:  Uremia,  von  Willebrand’s  disease,  drugs  
like  ASA,  NSAIDs….    
c.   COAGULOPATHIES  
o   Hereditary  
1.  Examples  :  Hemophilia,  Von  Willebrand’s  disease  
o   Acquired  
Ø  E.g  Vitamin  K  Deficiency  (FII,  VII,  IX,  X),                                                    
Hepatic  disorders  ,  DIC  ,  Inhibitors  of  coagulation,  
coagulopathy  of  trauma….  
 
 
 
 
 
 
 

 
 
8.   How  do  you  evaluate  a  preoperative  patient  clinically  for  the  
risk  of  bleeding  during  operation?    
 
ü  HISTORY  
o   Detailed  analysis  of  specific  bleeding  symptom  
§   mode  of  onset,  extent,  frequency  and  duration  of  bleeding  
episode  
§   triggering   event:   spontaneous,   trauma,   surgery,   menses,  
tooth  extraction,…  
§   site   or   location   of   bleeding:   mucocutaneous,   GIT,   GUS,  
airways,  joints,…    
o   The  presence  of  a  co  morbid  condition:    
§   liver   disease,   malignancy,   malabsorption,   HIV  
infection,  renal  disease,  SLE…  
o   Family   history   of   bleeding:   if   yes;   only   males   affected?  
Both  males  and  females  affected?  
o   Drug   history:   ASA   and   other   NSAIDs,   anticoagulants,  
antipletelet,   antibiotics,   hormone   therapy,   herbal  
medication…  
o   Nutritional   Hx:   excessive   alcohol   use,       the   amount   of  
vitamins  C  and  K  in  diet,  malnutrition…  
o   Gynecologic   and   obstetric   history:   AUB,   recurrent  
abortion  or  fetal  loss,  eclampsia,  preeclampsia  
ü  PHYSICAL  EXAMINATION  
o   Vital  signs  –  PR,  BP,…  severity  of  bleeding  
o    look  for  petichiae,  skin  bruises      
o   Look   for   complication   of   bleeding   like   anemia,   jaundice,  
neurologic   deficit,   joint   deformity,   compartment  
syndrome,  ….  

 
 
 o   Look   for   sign   of   underlying   co   morbid   disease   like   CLD,  
renal  failure,  malnutrition,  malignancy,  collagen  disorder,  
…..  
•   LABORATORY  EXAMINATION  
o   platlet  count,  PT  and  Aptt,  INR  
 

 
9.   Define;  discuss  causes,  diagnosis  and  mgt  of  DIC  
 
•   DIC   is   a   clinic-­‐pathologic   syndrome   characterized   by  
widespread   intravascular   fibrin   formation   in   response   to  
excessive   blood   protease   activity   that   overcomes   the   natural  
anticoagulant  mechanisms.  
 
 

 
 
 •    components  
o   Exposure of blood to procoagulants such as tissue factor and
cancer procoagulant
o   Formation of fibrin within the circulation
o   Fibrinolysis
o   Depletion of clotting factors
o   End-organ damage

•    
•  is  a   systemic   process   producing   both   thrombosis   and  
hemorrhage.  
•  Causes  
o  bacterial  sepsis  
o  Trauma  and  extensive  surgery    
o  malignant   disorders   such   as   solid   tumors   or   acute   promyelocytic  
leukemia,    
o  obstetric   causes:   e.g.   amniotic   fluid   embolism   and   abruptio  
placentae  
•   Mgt  
o   Treat  underlying  pathology  
o   Give  supportive  care:  
§   Fluids  
§   Vasopressor  agents  if  there  is  pump  problem    
§   Cardiac  or  ventilatory  assistance  
o   Monitor:  
§   PT,    INR,  aPTT,  Platelet  count  &  Fibrinogen  level  and  
FDP.  
§   If   the   PT   or   aPTT   is   prolonged   and   the   patient   is  
bleeding:  

 
 
 •      replace   with   the   freshest   whole   blood  
available   as   it   contains   fibrinogen   and   most  
other  coagulation  factors.  
•   give   FFP   as   this   contains   labile   coagulation  
factors:  1  pack/15  kg  body  weight    (4-­‐5  packs  
in  adults  
§   If   fibrinogen   is   low(<100   mg/dL)   or   brisk  
hyperfibrinolysis   ,   give   cryoprecipitate   (to   supply  
fibrinogen,  FVIII  and  vWF)  :  1  pack/6  kg  (8-­‐10  packs  
in  adults  
§   If  the  platelet  count  is  less  than  50  x  103/µL  and  the  
patient  is  bleeding  or  at  high  risk  of  bleeding  also  
give  platelet  concentrates:  4-­‐6  packs  

10.   How   do   you   prepare   a   patient   taking   anticoagulants   for  

surgery?  
 
Ø    Patients  taking  Heparin  
o   Elective  surgery  
§   UFH:  should  be  stopped  4-­‐6  hrs  before  surgery  
§   LMWH:  stop  24  hrs  before  planned  surgery  
§   Postop  resumption  
•   If  low  bleeding  risk  surgery:  24  hrs  post  procedure  
•   If  high  bleeding  risk  surgery:  48-­‐72  hrs  post  op  
o   Emergency  surgery  
§   Consider   reversal   with   IV   protamine   sulphate,   1  
mg/100IU.  (for  UFH)  
§   It  is  rarely  necessary  to  stop  low-­‐dose  heparin  injections,  
used   in   the   prevention   of   deep   vein   thrombosis   and  
pulmonary  embolism  prior  to  surgery.  

 
 
 Ø  Patients  taking  warfarin  
o   Elective  surgery:    determine  pre  procedure  INR  
§   If  2-­‐3:  stop  warfarin  for  5  days(  hold  4  doses)  
§   If  3-­‐4.5:  stop  warfarin  for  6  days(hold  5  doses)  
§   Target  INR  is  <  1.5  
§   In  patients  with  high  risk  for  thrombosis(e.g.  mechanical  heart  
valve),   UFH   can   be   substituted   for   warfarin,   with   cessation   of  
the   infusion   6   hours   before   surgery   or   use   LMWH   SC   to   be  
stopped  24  hrs  before  surgery.  
§   bridging anticoagulation should be considered in the following
groups of patients
•   Prior stroke or systemic embolic event
•   Active coronary or peripheral vascular disease
•   Previous thromboembolism during interruption of
warfarin therapy
•   Major cardiac or vascular surgery
§   Post-­‐op  Resumption  
•   Warfarin  therapy  should  be  restarted  12  to  24  hours  after  
surgery,  typically  the  evening  after  surgery,  provided  that  
surgical  hemostasis  has  been  achieved.  
•   With  heparin…  
o   Emergency  surgery  
§   Hold  warfarin  
§   Give  vitamin  K,  0.5-­‐2.0  mg  by  slow  IV  infusion.    
§   Give  fresh  frozen  plasma,  15  ml/kg  and  this  may  be  repeated  
to  bring  coagulation  factors  to  an  acceptable  range  
Ø   Patients  taking  Aspirin  
o   patients  at  low  risk  for  cardiovascular  events  who  are  receiving  aspirin  
therapy  should  stop  aspirin  7  to  10  days  before  surgery.  
o   Patients   believed   to   be   at   high   risk   for   perioperative   vascular  
complications   in   whom   perioperative   hemorrhage   would   result   in  
minimal  morbidity  should  continue  aspirin.  This  includes  patients  on  

 
 
 maintenance   aspirin   therapy   who   have   coronary   stents   or   who   are  
undergoing  CABG  or  peripheral  artery  surgery.  
o   Emergency??/??  
 
11.   list  the  causes  of  persistent  bleeding  during  an  operation    
 
12.   Pathophysiology  and  mgt  of  coagulopathy  of  trauma.  
 
—   the  key  initiators  to  the  process  of  ACoT  are  shock  and  tissue  injury.  

—   hypoperfusion  causes  activation  of  TM  on  the  surface  of  endothelial  cells.    

—   Thrombin-­‐TM  (thrombomodulin)  complexes  induce  an  anticoagulant  state  

through  activation  of  protein  C  and  enhancement  of  fibrinolysis.  
—   Management    
—   fresh  frozen  plasma,  packed  red  blood  cells,  and  platelets  (1:1:1  
ratios)  given  early  and  aggressively,  while  limiting  crystalloid  
—   Pharmaceutical  hemostatic  agents  
§   Recombinant  factor  VIIa  
§   Prothrombin  complex  concentrate  
§   Antifibrinolytic  therapy  
—   Monitoring    
o  serial  PT/INR,  PTT,  hemoglobin/hematocrit,  platelet  count,  
and  fibrinogen  levels  

o  Serial  measurements  of  arterial  blood  gas  for  pH  and  base  
deficit  are  indicated  for  monitoring  the  resolution  of  acidosis  
and  tissue  hypoperfusion  in  response  to  resuscitation.  
 

 
 
 1.  Why  do  we  need  rational  use  of  antibiotics?  
Irrational  use  of  antibiotics  is  a  global  problem  
o   Decrease  Drug  resistance  
o   Minimize  wastage  
o   Minimize  cost      
o   Decrease  side  effects  
o   Maintain  effectiveness  
o   .  
o   .  
o   .  
2.  Discuss  mechanisms  of  antibiotic  resistance.  
1.  Enzymatic:     MOs   produce   enzymes   that   destroy   the   active  
drug.     E.g.   Staph.   resistant   to   penicillin   G   produce   a   –
lactamase    
2.  Decreased  permeability:  MOs  change  their  permeability  to  
the  drug.    E.g.  Tetracyclines  accumulate  in  susceptible  
bacteria  but  not  in  resistant  bacteria  
3.  Efflux    
4.  Alteration  of  target  cells  
ü    Developing  an  altered  structural  target  for  the  drug    
E.g.  Erythromycin-­‐resistant  organisms  have  an  
altered  receptor  on  the  50S  subunit  of  the  ribosome    
5.  Development  of  an  altered  metabolic  pathway  that  
bypasses  the  reaction  inhibited  by  the  drug  
6.  Impaired  bind  up  of  antibiotics  
7.  Develop  an  altered  enzyme  that  can  still  perform  its  
metabolic  function  but  is  much  less  affected  by  the  drug.    
E.g.  trimethoprim-­‐resistant  bacteria  

 
 
 8.  Mutation    
3.  List  factors  for  selection  of  antibiotics.  
1.  Site  of  infection  
2.  Bactericidal  /static  
3.  Route  of  administration  
4.  Dosing  and  tissue  levels  
5.  True  presence  of  infection  (Topical)  
6.  Co-­‐morbid  conditions  
7.  Resistance  potential  
8.  Cost  and  availability  
9.  Pregnancy  
 
4.  Mention  causes  of  non  response  for  antibiotic  treatment.  
1.  Resistance    
2.  Incorrect  diagnosis  
3.  Choice  of  antibiotics  (Type,  Dose,  Route)  –  wrong  dose,  
route  or  drug  
4.  Abscess  
5.  Secondary  infection  
6.  Drug  interaction  
5.  List  characterstics  of  ideal  antibiotic.  
1.  Selective  toxicity  
2.  Soluble  in  tissue  fluids  
3.  Metabolized  slowly  
4.  Less  side  effect    
5.  Less  influence  on  normal  flora  of  the  host  
6.  Less  risk  of  drug  resistance  
7.  Low  cost  
 
 
 8.  Less  drug  interaction  
9.  Good  shelf  life  
10.   Should  not  be  easy  for  the  target  pathogen  to  establish  
resistance  against  an  antibiotic.    
 
 
6.  Describe  antibiotic  prophylaxis  and  mention  principles  of  
antibiotic  prophylaxis    
1.  Prophylaxis:    consists  of  the  administration  of  an  
antimicrobial  agent  or  agents  prior  to  initiation  of  certain  
specific  types  of  surgical  procedures  in  order  to  reduce  the  
number  of  microbes  that  enter  the  tissue  or  body  cavity.  
2.  Principles  of  antibiotic  prophylaxis  
ü   Single  dose  
ü   Should  be  given  within  1  hr  prior  to  incision  and  
not  more  than  for  24  hrs  
ü   Maximum  serum  level  during  procedure  
ü   Usually  at  the  time  of  incision  
ü   Narrow  spectrum  
ü   should  target  the  anticipated  organisms  
ü   unnecessary  if  the  patient  is  already  receiving  
antibiotics  that  cover  likely  pathogens  
ü   Repeat  dose  
o   For  procedures  lasting  more  than  four  hours.  
o   In  the  setting  of  major  blood  loss(20-­‐25ml/kg)  
o   Is  indicated  every  one  to  two  half-­‐lives  of  the  
drug  in  patients  with  normal  renal  function.  

 
 
 
  

7.  Why  do  people  use  antibiotics  irrationally?  

•   Lack  of  provider  knowledge  with  regard  to  prescription  
•   Prescriber  habit  
•   Poor  availability  of  drug  guidelines  and  bulletins  
•   Excessive  pharmaceutical  promotion  
•   Improper  diagnosis  
•   Patient  demand  in  reality  and  as  it  is  perceived  by  
subscribers  
•   Inappropriate  medicine  supply  
8.  Key  interventions  to  promote  more  rational  use(WHO)  

Educational,  Managerial,  Economic,  Regulatory  Strategies  

1.  Establishment  of  multidisciplinary  national  body  to  

coordinate  policies  on  medicine  
2.  Use  of  clinical  guidelines  
3.  Development  and  use  of  national  drug  list  
4.  Establishment  of  drug  and  therapeutic  committees  in  district  
hospitals  
5.  Inclusion  of  problem  based  pharmacotherapy  training  in  
undergraduate  curricula  
6.  Continuing  in-­‐service  medical  education  as  a  licensure  
requirement.  
7.  Supervision,  audit  and  feedback  
8.  Use  of  independent  information  on  medicines  
9.  Public  education  about  medicines  

 
 
 10.   Avoidance  of  perverse  financial  incentives.  
11.   Use  of  appropriate  and  enforced  regulation  
12.   Sufficient  government  expenditure  to  ensure  
availability  of  medicine  and  staff  
 

 
 

   

 
 
 1.  List  the  five  pillars  of  infection  control  
a.   Isolation  and  barrier  precautions  
b.  Decontamination  of  equipment  
c.   Prudent  use  of  antibiotics  
d.  Hand  washing  
e.   Decontamination  of  Environment  
2.  Mention  standard  precautions  
a.   Hand  hygiene  
b.  Use  of  personal  protective  equipment  (e.g.,  gloves,  gowns,  
facemasks,  goggle)                  
c.   Respiratory  hygiene  &  cough  discipline  
d.  Safe  injection  practices,    
e.   Safe  handling  of  potentially  contaminated  equipment  or  
surfaces.    

 
 
3.  what  is  sterilization  and  disinfection;  discuss  types  of  
sterilization.  
o   Disinfection:  application  of  antimicrobials  to  the  surface  of  
non-­‐  living  objects  to  destroy  microorganisms.    
o   It  does  not  necessarily  kill  all  microorganisms…  f.e.  Spores.  
§   High  level  disinfection:  Disinfectant  that  kills  all  
microbial  pathogens  except  large  numbers  of  bacterial  
spores.  It  is  used  for  items  involved  with  invasive  
procedures  that  cannot  withstand  sterilization.  
Ø  Eg  certain  types  of  endoscope,  surgical  
instruments  with  plastic  or  other  components  
that  cannot  be  autoclaved.  

 
 
 Ø    Aldehydes  (formaldehyde,  glutaraldehyde)  
Ø  H2o2  
Ø  Peracetic  acid  
Ø  Ozone  
§   intermediate  level  disinfectant  
o   Alcohols  
o   Phenolics    
o   Iodophore  compounds  
o   Chlorine  compounds  
§   low  level  disinfectant  
o   Are  used  to  treat  non  critical  instruments  &  device  
o   Antiseptics:  destroy  microorganisms  on  living  tissue  
o   Sterilization  :  refers  to  any  process  that  eliminates,  
removes,  kills,  or  deactivates  all  forms  of  life  and  other  
biological  agents.  
o   Methods  of  sterilization  
§   Heat,    
Ø  DRY  HEAT  
o   Flaming  
o   Incineration  
o   Hot  air  oven  
Ø  MOIST  HEAT  
o   Temp  <100  c  :  e.g.  pasteurization,  vaccine  
bath,  water  bath,  inspissations  
o   Temp  >100  c:  Autoclave/steam  under  
pressure  (121  c,  for  15  min,  15  Ibs)  
§   Chemicals  

 
 
 Ø  Formaldehyde  
Ø  Ethylene  oxide  
Ø  Betapropiolactone    
§   Irradiation  :  ionizing  or  non  ionizing  
§   High  pressure  &  filtration.    
 
Ø   Decontamination:  removes  pathogenic  microorganisms  from  
objects  so  they  are  safe  to  handle,  use,  or  discard.  
Ø   Cleaning:  is  the  removal  of  visible  soil  (e.g.,  organic  and  inorganic  
material)  from  objects  and  surfaces    
§   accomplished  manually  or  mechanically  using  water  with  
detergents  or  enzymatic  products..    
 
 
 

 
 
13.   Define  surgical  infections.  
 
o   Infections  requiring  surgical  interventions  or  
o   Infections  caused  by  surgical  interventions.  
 
14.   How  do  u  prevent  wound  infection  (surgical  infection)  
•   Pre-­‐operative  measures        
   
o   stop  smoking  at  least  30  days  before  surgery,  
o   nutritional  supplements  for  7  to  14  days  before  surgery  for  
severely  malnourished  
o   loosing  weight  :  for  elective  surgery  in  obese  pts    
o    Blood  glucose  control  in  diabetics    
o        In  bowel  surgery,  mechanical  and  chemical  preparation  of  the  
bowel  
o   Hair  removal  by  clipping  immediately  before  surgery  
o        Antibiotic  prophylaxis:  for  clean-­‐contaminated  or  contaminated  
procedures  in  which  the  risk  of  SSIs  is  high  or  in  procedures  in  
which  vascular  or  orthopedics  prostheses  are  used  
•   Intra  op  
o   hand  scrubbing  
o   a  thorough  skin  preparation  with  appropriate  antiseptic  
solutions  and  is  draped  in  a  sterile,  careful  fashion.  
o   Careful  handling  of  tissues  
o   Meticulous  dissection,  hemostasis,  and  débridement  of  
devitalized  tissue  
o   Compulsive  control  of  all  intraluminal  contents  
o   Preservation  of  blood  supply  of  the  operated  organs  
o   Elimination  of  any  foreign  body  from  the  wound  

 
 
 o   Maintenance  of  strict  asepsis  by  the  operating  team  (e.g.,  
no  holes  in  gloves,  avoidance  of  the  use  of  contaminated  
instruments,  avoidance  of  environmental  contamination,  
such  as  debris  falling  from  overhead)  
o   Thorough  drainage  and  irrigation  of  any  pockets  of  
purulence  in  the  wound  with  warm  saline  
o   Ensuring  that  the  patient  is  kept  in  a  euthermic  state,  
well-­‐monitored,  and  fluid-­‐resuscitated  
o   Expressing  a  decision  about  closing  the  skin  or  packing  
the  wound  at  the  end  of  the  procedure  
o        Operation  in  septic  areas  with  heavily    contaminated  
wounds  should  be  left  open  
o   Eradicating  dead  space  
o   Avoiding  inadvertent  entries  into  a  viscous    
o   Using  drains  and  suture  material  appropriately  
 
15.   How  do  u  manage  tetanus  prone  wound  
 

 
 
 
 
16.   List  classes  of  surgical  wounds  and  risk  of  SSI  

 
 
 
17.   Define  SSI  and  list  risk  factors  for  SSI.  
o   Surgical  site  infections  (SSIs)  are  infections  of  the  tissues,  
organs,  or  spaces  exposed  by  surgeons  during  performance  of  
an  invasive  procedure.  (within  30  days  of  the  procedure.)    
o   Incisional    
o   Superficial    
o   Deep    
o   Organ  Space    
o   Generalized  (peritonitis)    
o   Abscess    
o   Risk  factors  for  SSI.  
o   Patient  factors  
§   Older  age  
§   Immunosuppression  
§   Obesity  
 
 
 §   Diabetes  mellitus  
§   Chronic  inflammatory  process  
§   Malnutrition  
§   Smoking  
§   Renal  failure  
§   Peripheral  vascular  disease  
§   Anemia  
§   Radiation  
§   Chronic  skin  disease  
§   Carrier  state  (e.g.,  chronic  Staphylococcus  carriage)  
§   Recent  operation  
o   Local  factors  
o   Open  compared  to  laparoscopic  surgery  
o   Poor  skin  preparation  
o   Contamination  of  instruments  
o   Inadequate  antibiotic  prophylaxis  
o   Prolonged  procedure  
o   Local  tissue  necrosis  
o   Blood  transfusion  
o   Hypoxia,  hypothermia  
•   Microbial  factors  
o   Prolonged  hospitalization  (leading  to  nosocomial  
o   organisms)  
o   Toxin  secretion  
o   Resistance  to  clearance  (e.g.,  capsule  formation)  
o   Bacterial  

o   Perioperative  risk  factors  

o   Operative  site  shaving  

 
 
 o      Breaks  in  operative  sterile  technique  
o      Improper  antimicrobial  prophylaxis  
o      Prolonged  hypotension  
o      Contaminated  operating  room    
o      Poor  wound  care  postoperatively  
o      Hyperglycemia  
o    Wound  closure  technique  
 
18.   What  are  the  principles  you  would  follow  in  the  
management  of  surgical  infections?  
a.   Source  control    
o   drainage  of  all  purulent  material,  débridement  of  all  
infected,  devitalized  tissue,  and  debris,  and/or  removal  of  
foreign  bodies  at  the  site  of  infection,  plus  remediation  of  
the  underlying  cause  of  infection  
b.      Appropriate  use  of  antimicrobial  Agents    
o   Empiric  therapy    
o   Combination    
o   Duration:    
c.   Supportive:  wound  care,  pain  management,  dvt  prophylaxis,  
nutrition,  early  mobilization  
d.  ICU    
e.   Block  inflammatory  mediators    
f.   Standardize  wound  debridement    
g.   Improve  patient’s  systemic  conditions  and  management  of  
chronic  diseases    
h.  Specific  immune  therapy    
 
 
 

 
 
 4.  Discuss  briefly  the  principles  of  pre-­‐op  management  in  
major  surgery.  
 

The  main  aim  of  pre-­‐operative  patient  evaluation  is  to  identify  and  quantify  any  comorbidity  that  may  
affect  the  operative  outcome.  

Pre-­‐operative  evaluation  of  patients  should  help  as  in  knowing  patient’s  

-­‐   General  health  assessment  

-­‐   ASA  classification  
o   1  =A  normal  healthy  patient  
o   2  =A  patient  with  a  mild  systemic  disease  
o   3  =  A  patient  with  a  severe  systemic  disease  that  limits  activity,  but  is  not  incapacitating  
o   4  =A  patient  with  an  incapacitating  systemic  disease  that  is  a  constant  threat  to  life  
o   5  =A  moribund  patient  not  expected  to  survive  24  hours  with  or  without  operation  
-­‐    
-­‐   Grade  of  surgery    

o    
-­‐   Malampati  Grade  

 
 
 o    

 
A.  General  health  assessment  
•   History  
ü  Age  
ü  Risk  factors  for  anesthesia  
o   CVS  
§   High  risk  
•   Type  of  surgery  
o   Thoracic,  upper  abdominal,  
neurological  &  major  
orthopedics  
o   Vascular  surgery  
•   Recent  MI  
•   Heart  failure  
•   Hypertension  
•   Anemia  
•   Dyspnoea  
•   DVT  
•   Valvular  heart  disease,    
•   Any  cardiac  illness  

 
 
  
o   Respiratory  
§   Smoking  :  for  at  least  4  to  8  weeks  
§   Asthma  
§   Chronic  cough  
§   COPD  
§   New  sputum  production  
o   Endocrine  
§   Hypertension  
§   Diabetes  
§   Pheochromocytoma  
o   Renal  
§   Renal  disease    
§   Use  of  diuretics  &  digitalis  
o   Neurologic  
§   Epilepsy  
§   CVA/  stroke    
§   TIA  
o   Drug  Hx  
o   Alcohol  Hx  
o   Previous  anesthetic  Records  
o   Bleeding  tendency  
o   Nutritional  history  
o   Recent  weight  loss-­‐    
o   5%  in  one  month  or  10%  in  six  months  
o   Changes  in  eating  or  bowel  habit  
o   Changes  in  abdominal  girth,  changes  in  belt  size,  or  
clothing  
o   Loss  of  muscle  bulk  
o   Leg  swelling-­‐  why?    

 
 
  
•   Physical  Examination:  including  functional  asst.  
ü   HEENT:  malampati  
ü   Respiratory:  FEV1,  FVC,  and  DCO  
ü   CVS:  flight  of  stairs  test  
•   Lab  tests  
ü   Routine  
o   CBC  
o   Blood  group  &  Rh    
o   U/A  
ü  Specific  lab  tests  based  on  pts  condition  
 

 
 
                
 

5.   Why  should  diabetes  be  controlled  preoperatively?  

 
ü  Diabetes  has  an  impact  on:  
a.   Perioperative  fluid  and  electrolyte,    
b.  Nutritional  balance;    
c.   Cardiovascular  and  renal  function;  
i.   Coronary  heart  disease,  silent  ischemia…  
d.  Immunity  and  wound  healing,  especially  when  the  condition  is  
poorly  controlled  
 
6.  Outline  briefly  the  management  of  a  patient  with  
Diabetes  mellitus  before  surgery.  
 
 
  
History  should  include:  
a.   Type  and  treatment  of  diabetes  or  insulin  resistance  
b.  Compliance  to  treatment  and  glycemic  control  
c.   Known  complications  and  previous  hospitalizations  
d.  The  course  and  complications,  if  any,  of  prior  surgeries.  
e.   Symptoms  of  ischemic  cardiac,  renal,  and/or  peripheral  vascular  
disease,  if  any.    
 
Routine  physical  examination:  
f.   Complete  cardiac  evaluation  
g.   Identify  and  treat  hypertension.    
h.  Status  of  the  peripheral  circulation/the  sensory  nerves.    
i.   Neuropathy  by  evaluating  for  the  presence  of  orthostatic  
hypotension.    
 
Laboratory:  
j.   Routine  screening  
k.   Fasting  sugar  level  and  hemoglobin  A1c.    
l.   BUN  and  creatinine,    microalbuminuria  and  proteinuria    
m.  EKG  
 
Goals  of  glycemic  control  

n.  Maintenance  of  fluid  and  electrolyte  balance  

o.  Prevention  of  ketoacidosis    
p.  Avoidance  of  marked  hyperglycemia    
q.  Avoidance  of  hypoglycemia  
 
r.   Glycemic  target:  RBS:  below  180  to  200  mg/dL,  FBS<140  
 
s.   Types  of  diabetic  patients  
 
 
 
 •   Type  1  DM  on  insulin  
•   Type  2  DM  on  dietary  management  
ü   No  treatment  needed  preoperatively  
ü   If  needed  use  short  acting  supplemental  insulin  
intraop  if  patients  go  hyperglycemic  intraop  
•   Type  2  DM  with  Oral  agents  
ü   Continue  usual  drugs  until  morning  the  day  of  
surgery  except  metformin  
ü   Use  short  acting  agents  intraop  
ü   Continue  Oral  agents  post  op  
•   Type  2  DM  on  insulin  
ü   Continue  usual  dose  till  the  night  of  surgery,  give  
rd
2/3  of  usual  dose  the  night  before  surgery  and  half  
the  usual  morning  dose  the  morning  of  surgery.  
ü   Start  5%  dextrose  infusion  in  the  morning  of  
surgery  
ü   Keep  short  acting  insulin  for  acute  controle.  
 
t.   The  following  recommendations  can  serve  as  a  general  guide:  
i.   Plan  to  schedule  the  surgery  as  the  first  case  of  the  day  to  prevent  
prolonged  fasting.  
ii.   During  surgery,  a  standard  5%  or  10%  dextrose  infusion  is  used  with  
short-­‐acting  insulin  or  an  insulin  drip  to  maintain  glycemic  control    
iii.   As  a  general  rule,  oral  hypoglycemic  agents  are  held  on  the  day  of  
surgery  to  avoid  reactive  hypoglycemia.  The  exception  is  metformin,  
which  should  be  held  for  at  least  24  hours  preoperatively  to  avoid  
the  risk  drug-­‐induced  lactic  acidosis.  
iv.   Insulin  should  be  continued  through  the  evening  before  surgery,  
including  the  usual  dose  of  insulin  glargine  (Lantus).  
v.   Type  1  diabetics  should  be  continued  on  basal  insulin  replacement  
even  while  nothing  by  mouth  status  to  prevent  ketoacidosis.  
Administer  half  the  usual  morning  dose  of  intermediate-­‐  or  long-­‐

 
 
 acting  insulin  after  arrival  to  the  surgery  center,  but  hold  the  usual  
dose  of  rapid-­‐  or  short-­‐acting  insulin.  
vi.   Use  the  patient's  own  sliding  scale  to  administer  a  short-­‐acting  
insulin  subcutaneously  to  maintain  the  glucose  between  100  and  200  
mg/dL  prior  to  the  scheduled  surgery.  

 
7.  Outline  briefly  the  management  of  a  patient  with  HPN  
before  surgery.  
 
-­‐   Hypertension  is  a  chronic  disease  where  patients  can  be  in  one  of  the  following  groups  
1.   Patient  with  Controlled  Hypertension  on  chronic  anti-­‐hypertensive  therapy  for  elective  surgery  
or  emergency  
2.   Patient  with  uncontrolled  hypertension  for  elective  surgery  
3.   Patient  with  uncontrolled  hypertension  for  emergency  surgery  

 
 
  
         

 
 
 
 
•   Target    
•   The  ideal  circumstance  is  to  normalize  blood  pressure  (eg,  to  less  
than  140/90  mmHg)  for  several  months  prior  to  elective  surgery.  
However,  it  is  not  necessary  to  postpone  elective  procedures  in  
patients  with  a  blood  pressure  below  170/110  mmHg  .  
ü   Hold  diuretics    on  the  morning  of  surgery  
o   Since  diuretics  may  increase  the  risk  of  hypotension  if  continued  on  
the  morning  of  surgery.  
ü   Elective  surgery  should  be  postponed  in  patients  with  blood  pressures  
above  170/110  mmHg.  Such  patients  who  require  urgent  surgery  should  be  
treated  with  a  parenteral  drug  acutely.  
8.  Discuss  preoperative  assessment  of  a  patient  for  
pulmonary  risk.  
§   Patient  related  risk  factors  
o   include  the  following:    
§   Age    
§   Chronic  lung  disease    

 
 
 §   Asthma    
§   Smoking    
§   General  health  status    
§   Obesity    
§   Obstructive  sleep  apnea    
§   Pulmonary  hypertension    
§   Heart  failure    
§   Upper-­‐respiratory  infection    
§   Metabolic  factors    
§   Procedure  related  risk  factors  
o   Surgical  site:  upper  abdominal  and  thoracic  
o   Type  of  surgery:  elective  vs  emergency  
o   Duration  of  surgery    
o   Type  of  anesthesia    
o   Type  of  neuromuscular  blockade    
 
Assessment    
 
•   History  
–   Any  history  suggesting  unrecognized  chronic  lung  disease  or  heart  
failure,  such  as  exercise  intolerance,  unexplained  dyspnea,  or  cough,  
requires  further  consideration.  
•   P/E  
–   should  be  directed  toward  evidence  for  obstructive  lung  disease,  
especially  noting  decreased  breath  sounds,  wheezes,  rhonchi,  or  
prolonged  expiratory  phase  .    
–   In  addition,  measurement  of  oxygen  saturation  by  oximetry  helps  to  
stratify  risk  and  is  useful  before  high-­‐risk  surgeries  
•   All  candidates  for  lung  resection  should  have  preoperative  pulmonary  
function  tests  performed.  
•   Potential  preoperative  laboratory  tests  include  the  following:    
–   Pulmonary  function  tests  (PFTs)    

 
 
 –   Arterial  blood  gas  analysis    
–   Chest  radiographs    
–   Exercise  testing    
•   In  patients  undergoing  high-­‐risk  surgery  who  are  over  age  50  years,  or  who  
have  cardiac  or  pulmonary  disease  suggested  by  the  clinical  evaluation,  a  
chest  radiograph  within  the  past  six  months  is  needed.  Pulmonary  function  
tests  should  be  reserved  for  patients  with  uncharacterized  dyspnea  or  
exercise  intolerance  and  for  those  with  COPD  or  asthma  where  clinical  
evaluation  cannot  determine  if  airflow  obstruction  has  been  optimally  
reduced.  The  benefit  of  PFTs  in  other  situations  is  unproven.  There  is  no  
role  for  preoperative  arterial  blood  gas  analyses  to  identify  high-­‐risk  
patients  or  to  deny  surgery.  
 
 
 
 
9.  Strategies  to  reduce  postoperative  pulmonary  
complications  
PREOPERATIVE  STRATEGIES  
a.   Smoking  cessation  as  early  as  possible;  cessation  for  eight  weeks  or  
longer  is  likely  of  greater  benefit    
b.   Inhaled  ipratropium  or  tiotropium  for  all  patients  with  clinically  
significant  COPD    
c.   Inhaled  beta-­‐agonists  for  patients  with  COPD  or  asthma  who  have  
wheezes  or  dyspnea    
d.   Preoperative  glucocorticoids  for  patients  with  COPD  or  asthma  who  are  
not  optimized  and  whose  airway  obstruction  has  not  been  maximally  
reduced    
e.   Delay  elective  surgery  if  respiratory  infection  present    
f.   Antibiotics  only  for  patients  with  lower  respiratory  tract  infection.  
Elective  surgery  should  be  cancelled  until  such  treatment  is  completed.  
g.   Preoperative  inspiratory  muscle  training    

 
 
 h.   Preoperative  chest  physical  therapy    
i.   Patient  education:    Lung  expansion  maneuvers  such  as  coughing,  
incentive  spirometry,  and  voluntary  deep  breaths  are  best  taught  prior  to  
surgery  
INTRA  OPERATIVE  —  The  following  intraoperative  interventions  are  definitely  
beneficial:    
j.   Choose  alternative  procedure  lasting  less  than  three  to  four  hours  when  
possible    
k.   Surgery  other  than  upper  abdominal  or  thoracic  when  possible    
l.   Regional  anesthesia  (nerve  block),  when  this  is  an  option,  in  very  high-­‐
risk  patients    
m.  Avoid  use  of  pancuronium  as  a  muscle  relaxant  in  high-­‐risk  patients    
Choosing  laparoscopic  rather  than  open  abdominal  surgery  when  possible  
may  be  beneficial.    
Epidural  or  spinal  anesthesia  may  confer  lower  risk  than  general  anesthesia,  
though  this  remains  an  area  of  debate.    
Perioperative  pulmonary  artery  catheterization  is  not  beneficial  
 
•   POSTOPERATIVE  STRATEGIES      
–   include  lung  expansion  maneuvers,  adequate  pain  control,  and  
potentially,  respiratory  stimulants.    
–   lung  expansion  maneuvers  
•   chest  physical  therapy,  deep  breathing  exercises,  incentive  
spirometry,  intermittent  positive  pressure  breathing,  and  
continuous  positive  airway  pressure  (CPAP).  
•   These  maneuvers  increase  lung  volumes  after  surgery  through  
inspiratory  effort.  
–   Pain  control      
•   Adequate  postoperative  pain  control  may  help  to  minimize  
postoperative  pulmonary  complications  by  enabling  earlier  
ambulation  and  improving  the  patient's  ability  to  take  deep  
breaths  
•   Postoperative  pain  control  has  been  consistently  improved  
with  epidural  analgesia  compared  with  parenteral  opioids    
•   Intercostal  nerve  blocks  
–   Routine  use  of  nasogastric  tube  decompression  after  abdominal  
surgery  increases  the  risk  of  postoperative  pulmonary  complications.    

 
 
  
10.  Pre-­‐op  DVT  prophylaxis  
a.   Varicose  veins  
b.   High  oestrogen  pill  
c.   Obesity  
d.   Previous  DVT  or  PE  
e.   Age  >40  years  
f.   Malignancy    
g.   Infection  
h.   Heart  failure  /  recent  infarction  
i.   Polycythaemia  /thrombophilia    
j.   Immobility  (  bed  rest  over  4  days)  
k.   Major  trauma  
 

 
 

 
 
  
 

 
 
19.   Enumerate  causes  of  postop  fever.  
 
Infectious  
n   Surgical  site  infection  
n   Pneumonia      
n   Urinary  tract  infection  
n   Intravascular  catheter-­‐associated  infection  
n   Antibiotic-­‐associated  diarrhea    
n   Sinusitis    
n   Otitis  media  
n    Parotitis    
n   Intraabdominal  abscess  
n   Meningitis  
n   Acalculous  cholecystitis    
 
Non  infectious  
•   Surgical  site  inflammation  without  infection  
n   Hematoma/seroma  Suture  rxn  ,  Thrombosis    
n   DVT,PE    
•   Inflammatory    
n   Pancreatitis    
•   Vascular    
n   Subarachnoid  hemorrhage  Myocardial  infarction  Bowel  
ischemia/infarction    
•   Other    
n   Medications  Drug/alcohol  withdrawal    
n   Transfusion  rxn,  
 
 
 
 
 
 
 
 

 
 
  
 
DDX  OF  POST  OP  FEVER  

 
 
 
20.   What  is  the  care  taken  in  the  immediate  postop  period.  
Indicate  the  most  common  complications  in  this  period  and  
outline  their  management.  

 
 
  
21.   Discuss  briefly  postop  pulmonary  complications.  
 
a)  Atelectasis  
b)  Pneumonia  
c)   Aspiration  pneumonitis  
d)  Pulmonary  edema,  ALI,  ARDS  
e)  Pulmonary  embolism  
 
22.   Discuss  methods  to  prevent  Post  operative  infections  
 
•   See  surgical  infections  
•   Please  hear  me.    DAWIT  G/G  

 
 
1.  List  characteristics  of  Malignancy    

     
2.  Explain    the  Clinical  implications  of  Gomepertizan  curve            
Some details about Gompertzian…actuary
The Gompertzian curve describes the growth of a typical tumour. In its
early stages, growth is exponential but, as the tumour grows, the growth
rate slows. This decrease in growth rate probably arises because of
difficulties with nutrition and oxygenation. The tumour cells are in
competition: not only with the tissues of the host, but also with each
other.  
 

 
 
    

 
3.  Identify    The  Pros  and  cons    of  Screening    

 
 
 •   Screening   is   detection   Of   disease   in   Asymptomatic  
population  to  improve  out  come  by  early  Diagnosis  
•   The  Biases  of  Screening    
o   Lead  time  Bias  
§   Early  dictation  will  improve  out  come  ???  
§   Lead  time  bias  describes  the  phenomenon  whereby  early  
detection  of  a  disease  will  always  prolong  survival  from  
the  time  of  diagnosis  when  compared  with  disease  picked  
up  at  a  later  stage  in  its  development  whether  or  not  the  
screening   process   has   altered   the   progression   of   the  
tumour  
o   Selection  Bias  
§   Selection  bias  
§   describes   the   finding   that   individuals   who   accept   an  
invitation   for   screening   are,   in   general,   healthier   than  
those  who  do  not.  It  follows  that  individuals  with  screen-­‐
detected   disease   will   tend,   independently   of   the  
condition  for  which  screening  is  being  performed,  to  live  
longer.  
§   Individuals   agreeing   for   screening   and/or   come   for  
screening  have  better  health  and  live  longer.  
•   Length  Bias  
o   Slowly  growing  tumor  may  be  picked  up  more  commonly  than  
aggressive  tumors  giving  chance  for  screening    
o   Length   bias   is   brought   about   by   the   fact   that   slow-­‐growing  
tumours  are  likely  to  be  picked  up  by  screening,  whereas  fast-­‐
growing  tumours  are  likely  to  arise  and  produce  symptoms  in  
between  screening  rounds.  Thus,  screen-­‐detected  tumours  will  
tend  to  be  less  aggressive  than  symptomatic  tumours.  

 
 
Because  of  these  biases,  it  is  essential  to  carry  out  population-­‐based  randomized  
controlled  trials  and  to  compare  a  whole  population  offered  screening  (including  
those  who  refuse  to  be  screened  and  those  who  develop  cancer  after  a  negative  
test)  with  a  population  that  has  not  been  offered  screening.  This  research  design  
has  been  applied  to  both  breast  cancer  and  colorectal  cancer:  in  both  cases,  there  
was  reduction  in  disease-­‐specific  mortality.  
 
 
 
 
 
 
 
 
 
4.  List  Down  the  criteria  for  screening  

 
5.  Discuss    the  modes  of  management  of  malignancy    
•   Surgery    
•   Radiotherapy    
•   Chemotherapy    
 
 
 •   Biological  therapy    
 
6.  Discuss  the  role  of  Surgery  in  the  management  of  malignancy    
•   Treat  the  primary  cancer  
•   Treat  complication  
•   To  remove  isolated  metastatic  masses  
•   Debulking    
•   Prevention  
•   Surgical  removal  of  a  source  of  hormone  
•   Palliation    
•   Diagnosis  and  Staging  
•   Reconstruct   anatomical   defects   to   improve   function,   cosmetic  
appearance,  and  quality  of  life  
•   providing   access   for   chemotherapy   delivery   (implanted   infusion  
pumps)  
 
 
 
 
 

 
 
 1.  What  is  Anesthesia  ?  
•   It  is  a  pharmacologically  induced  and  reversible  state  of  
amnesia,  analgesia,  loss  of  responsiveness,  loss  of  skeletal  
muscle  reflexes  or  decreased  stress  response,  or  all  
simultaneously    
 
2.  Anesthetic  techniques  
•   General  anesthesia  
i.                        Inhalation  
ii.                        Parenteral    
•   Regional  anesthesia  
•   Regional  analgesia  
•   Local  anesthesia  
•   Conscious  Sedation  (monitored  anesthesia  care)  
 
3.  Define,  list  components,  phases,  and  methods  of  GA  
•   GA:      reversible,  drug-­‐induced  loss  of  consciousness    during  which  
patients  are  not  arousable,  even  by  painful  stimulation.      
•   Components  
o   Unconsciousness/amnesia  
o   Analgesia    
o   Muscle  relaxation(-­‐+)    
•   Phases  
•   Induction:    
o   before  giving  any  induction  drug  patients  has  to  be  
oxygenated  atleast  for  2-­‐3  minutes  by  holding  the  mask  
close  to  the  face  
o   IV  or  Inhalational  
o   IV:  faster(  10–20  seconds  to  induce  total  
unconsciousness)  e.g.  ketamine,  thiopental,  opioids,  
propofol  
 
 
 o   Inhalational:    
§   When  IV  access  is  difficult  
§   Difficulty  maintaining  airway  
§   Controlled  reversibility  
§   Pt  preference…children  
o   When  we  make  sure  that  we  can  ventilate  the  patient  a  
short  acting  muscle  relaxant  will  be  given  and  proceed  
to  intubation    

•   Maintenance  
o   reqires  an  anesthetic  mixture  to  keep  the  patient  asleep  
and  a  relaxant  to  keep  the  patient  paralized  and  
ventilated  
o   IV  or  Inhalational  or  combination.  
o   Combination  is  commonly  used.  
o   Halothane  with  opiods  for  maintenance  and  long  acting  
muscle  relaxants  like  pancronium,  vecronium    
o    
•   Recovery/Emergence  
o   As   the   operation   comes   to   end   the   concentration   of  
anesthetics  is  decreased  and  patient  is  allowed  to  breath  
o   A  reversal  has  to  be  given  atropine(protect  the  heart  by  
acting  on  muscarinic  receptors)  with  neostigmine(reverse  
the  action  of  muscle  relaxants  )  
4.  Complications  of  GA  
 
•   Failed  intubation  
•   One  lung  intubation  
•   Delayed  awakening  
•   Use  of  multiple  drugs  
•   Death  
•   CVS  
i.   Cardiac  arrest  
 
 
 ii.   MI  
•   R/S  
i.   Aspiration    
ii.   Difficult  intubation                                                                                                                                                                      
n  
•   NS  
•  POCD  
•  Post  op  delirium  
•    accident    
•   Miscellaneous      
•  Anaphylaxis  
•  PONV  
•  Sore  throat    
•  Drowsiness  
•  Malignat  hypertention  
•  Headache    
•  Dental  damage  
 
5.  Define  Regional  anesthesia  and  outline  types,  
advantages  and  complications  of  RA.  
•   Defn.    Local  anesthetics  applied  around  a  peripheral  
nerve  at  any  point  along  the  length  of  the  nerve  from  
spinal  cord  up  to  the  nerve  endings  for  the  purposes  of  
reducing  or  preventing  impulse  transmission.  
•   Types    
o   Topical  
o   Local/Field  
o   Intravenous  block  (“Bier”  block)  
o   Peripheral  (named)  nerve,  e.g.  radial  n.  
Femoral  

 
 
 o   Plexus  -­‐  brachial,  lumbar  
o   Central  neuraxial  -­‐  epidural,  spinal  
•   Advantages  :    
o   Blunt  the  “stress  response”  to  surgery    
o   Decrease  intraoperative  blood  loss    
o   Lower  the  incidence  of  postoperative  
thromboembolic  events    
o   Decrease  morbidity  and  mortality  in  high-­‐risk  
surgical  patients    
o   Can  be  used  to  extend  analgesia  into  the  
postoperative  period    
o   Cost  
o   Patient  satisfaction    
o   few  adverse  effects  on  the  respiratory  system    
o   reduced  risk  of  airway  obstruction  or  the  
aspiration  of  gastric  contents  
o   rapid  recovery  and  absence  of  side  effects.  
o   Diabetic  patients.  There  is  little  risk  of  
unrecognised  hypoglycaemia  in  an  awake  patient  
o   Early  mobilization  and  hospital  discharge  
o   Increases  attachment  of  mother  to  child    
6.  Short  note  on  spinal  and  epidural  anesthesia  
•   Spinal  anaesthesia    is  a  form  of  regional  anaesthesia  
involving  injection  of  a  local  anaesthetic  into  the  
subarachnoid  space    
i.   Spinal  anaesthetics  are  typically  limited  to  
procedures  involving  most  structures  below  the  
umblicus    
ii.   Bubivacaine  0.5%  (3-­‐4  ml  for  spinal  anesthesia)    has  
total  duration  of  action  of  60-­‐90mns  with  out  
adrenaline  and  upto  3hrs  with  adrenaline  

 
 
 iii.   Lidocaine  5%  (1-­‐2ml  for  spinal  anesthesia)  :  duration  
of  action  of  30mns  with  out  adrenaline  and  60mns  
wit  adrenaline  
iv.   Contra  indications  
§   Non-­‐availability  of  patient's  consent  
§   local  infection  or  sepsis  at  the  site  of  lumbar  
puncture  
§    bleeding  disorders  
§    space  occupying  lesions  of  the  brain  
§   disorders  of  the  spine    
§    hypotension    
 
v.   Complications  
§   Spinal  shock  
§   Cardiac  arrest  
§   Broken  neddle  
§   Bleedingà  hematomaàcompression  of  spinal  
nerves  
§   Infection  
§   Post  Spinal  headache  
 

 
•   Epidural  Anaesthesia    
i.   Given  in  a  potential  space  that  lies  between  the  dura  
and  the  periosteum  lining  the  inside  of  the  vertebral  
canal  which  extends  from  the  foramen  magnum  to  
the  sacral  hiatus    
ii.   The  advantage  of  epidural  over  spinal  anesthesia  is  
the  ability  to  maintain  continuous  anesthesia  after  
placement  of  an  epidural  catheter,  thus  making  it  
suitable  for  procedures  of  long  duration  

 
 
 iii.   The  disadvantage  of  epidural  over  spinal  is  that  it  is  
difficult  to  find  the  space  and  since  it  is  a  big  space  
we  have  to  use  10  times  the  volume  of  local  
anesthetic  that  we  use  in  spinal  anesthesia    
 
 
7.                          Structures  to  be  encountered  during  spinal  
anesthesia  
•   Skin  
•   subcutaneous  tissue    
•   Fat  
•   Supraspinous  ligament  
•   Interspinous  ligament  
•   Ligamentum  flavum    
•   Dura  
•   Arachinoid    
•   Pia  mater    
 
8.    What  is  Premedication?  
 
§   Is  adminstration  of  drugs  before  operation  with  the  
general  aims  of  lessening  anxiety  and  fear,  to  reduce  the  
volume  and  acidity  of  gastric  contents  and  to  reduce  
secretions.  
§   Reasons  for  prescribing  premedications  include  
Patient-related reasons:
§   1. Sedation: decrease anxiety
§   2. Amnesia
§   3. Analgesia
§   4. Antisialogogue effect (to dry oral secretions)
§   5. Medications to decrease gastric acidity and gastric volume.

 
 
 §   6. T o facilitate induction of anaesthesia.
Procedure-related reasons:
§   Antibiotic prophylaxis to prevent infective endocarditis in susceptible
patients.

§   Gastric prophylaxis (to minimize the risk of gastric aspiration during an-
aesthesia).

§   Corticosteroid coverage in patients who are immunosuppressed

§   To avoid undesired reflexes arising during a procedure

§   Anticholinergic agents to decrease oral secretions and facilitate a planned

awake intubation with a fiberoptic bronchoscope.

§   Examples: Diazepam, lorazepam, midazolam, Hyocine, Morphine, atropine,

Promethazine

9.  Preanesthetic  evaluation  
o   History  
o   Anesthetic  
§   Any  problems  encountered  during  past  anestetics  
must  be  fully  investigated  
§   Family  anesthetic  history  is  also  important  
•   Eg  Succinyl  Choline-­‐  malignant  hyperthermia…  
runs  in  family.    
o   Medical  
§    respiratory  problems  ;cough  ,smoking  ,breathlessness  
,exercise  tolerance  history  of  previous  chest  problems  
(TB  ,bronchitis)  
§    cardiovascular  disease  ;  difficulty  in  breathing  
,palpitation  ,chest  pain  ,previous  heart  attacks  
,hypertension  
o   Other  illnesses  
§   Diabetes  mellitus  ,renal  disease  ,allergies  to  drugs  
,plasters    
 
 
 o   Surgical    
§   past  surgical  procedures  as  well  as  that  for  which  the  
patient  is  being  assessed  
o    drug  history  
§   steroids  
§      antihypertensives    
§    betablockers    
§    diurtics    
o   P/E  
o   General  examination  
o   Airway  examination  
§   note  any  anatomical  features  that  would  hinder  the  
maintenance  of  a  clear  airway  or  interfere  with  endotracheal  
intubation  [Link]  neck  ,protruding  teeth,large  tongue.  
§   Evaluation  of  the  airway    
•   determination  of  the  thyromental  distance,    
•   the  ability  to  flex  the  base  of  the  neck  and  extend  the  
head,    
•    examination  of  the  oral  cavity,  including  dentition  
•   The  Mallampati  classification  has  become  the  standard  
for  assessing  the  relationship  of  the  tongue  size  relative  
to  the  oral  cavity  
o   Systemic  exam  
LAB  

•   Atleast  every  patient  coming  to  the  theater  should  have  Hct  and  blood  
group  
•   Other  investigations  depends  on  the  clinical  condition  of  the  patient  ,age  
and  type  of  surgery  
•   Age  >  60  yrs  ECG  and  chest  x-­‐ray    
Fasting  guidelines  
o   for  elective  surgery  
o   patients  should  be  kept  NPO(  nothing  per  mouth  )  for  solid  
foods  atleast  6  hrs  and  liquid  for  2  hrs  before  surgery  

 
 
 o   For  babies  and  small  children  breast  milk  may  be  allowed  up  to  
4  hrs  and  water  until  2  hrs  before  surgery    
o   For  emergency  surgery    
o   all  emergency  patients  and  laboring  mothers  should  be  
considered  as  full  stomach  and  prequations  should  be  taken  to  
avoid  aspiration    
10.   Ideal  Anesthetic  Agent    
 

•   Drug  compatibility  and  stability  in  solution.  

•   Lack  of  pain  on  injection,  venoirritation,  or  local  tissue  damage  
from  extravasation.  
•   Low  potential  to  release  histamine  or  precipitate  hypersensitivity  
reactions.  
•   Rapid  and  smooth  onset  of  hypnotic  action  without  excitatory  
activity.  
•   Rapid  metabolism  to  pharmacologically  inactive  metabolites.  
•   A  steep  dose-­‐response  relationship  to  enhance  titratability  and  
minimize  accumulation.  
•   Lack  of  acute  cardiovascular  and  respiratory  depression.  
•   Decreases  in  cerebral  metabolism  and  intracranial  pressure.  
•   Rapid  and  smooth  return  of  consciousness  and  cognitive  skills  with  
residual  analgesia.  
•   Absence  of  postoperative  nausea  and  vomiting,  amnesia,  
psychomimetic  reactions,  dizziness,  headache,  or  prolonged  
sedation  (“hangover”).    
 
11.   Doses  of    LA  
                                                     Dose-­‐  
               Lidocaine    5  mg/kg  
                                                   -­‐  7mg/kg  (Adr.)    
             Bupivacaine    
                                                   -­‐  2mg/kg  

 
 
 12.  Rapid  sequence  intubation  
  The goal of rapid sequence induction is to achieve secure protection of the airway
with a cuffed endotracheal tube while preventing vomiting and aspiration.

Rapid sequence induction is performed as follows:

•   Proceed only after evaluation of the airway predicts an uncomplicated intubation.

•   Preoxygenate the patient.
•   Rapidly introduce an IV induction agent (e.g., propofol).
•   An assistant to the anesthesiologist presses firmly down on the cricoid cartilage to
block any gastric contents from being regurgitated into the trachea, a muscle
relaxant is injected, and the trachea is quickly intubated.
•   The assistant is instructed not to release pressure on the cri- coid cartilage until the
cuff of the endotracheal tube is inflated and the position of the tube is confirmed.

 
                     
 
 
 
 
 
       
 
 

 
 
1.  List  effects  of  malnutrition.  
o   Impaired  wound  healing    
o   Impaired  immunity    
o   Higher  incidence  of  post-­‐op  complications:  high  incidence  of  
operative  complications  and  death  ~  30%  
o   Impaired  muscle  function  (including  cardiac  and  respiratory  
muscles)    
o   Impaired  GI  structure  and  function    
o   Deterioration  in  mental  function    
o   Association  with  increased  length  of  stay  and  increases  costs    
 
2.  List  metabolic  responses  to  starvation.  
The  body’s  response  to  starvation  is  to    

•   Decrease  body’s  BEE  

•   Change  in  fuel  consumption  
•   Relative  sparing  of  proteins  
•   After  a  short  fast  lasting  12  hours  or  less,  most  food  from  the  
last  meal  will  have  been  absorbed.    
•   Plasma  insulin  levels  fall  and  glucagon  levels  rise,  which  
facilitates  the  conversion  of  liver  glycogen  into  glucose.  
•   followed  by  muscle  glycogen.  
•   Carbohydrate  stores  are  exhausted  after  a  24-­‐hour  fast  
•   In  the  first  few  days  of  starvation,  caloric  needs  are  supplied  by  
fat  and  protein  degradation  with  fat  predominance    
•   Most  of  the  available  protein  is  from  breakdown  of  skeletal  and  
visceral  muscle.    
•   Protein  is  converted  to  glucose  via  hepatic  gluconeogenesis.    
 
 
 •   Within  approximately  10  days  of  starvation,  the  brain  adapts  to  
use  fat  as  its  fuel  source.  Because  the  brain  cannot  use  free  
fatty  acids  in  the  same  manner  as  other  tissues  do,  it  relies  on  
ketoacids  produced  by  the  liver.  
•   Most  important  point:  relative  sparing  of  protein  during3-­‐
10days,  usage  of  ketoacids  by  the  brain  suppresses  proteolysis.  
this  inhibitory  mechanis  is  suppressed  in  trauma  and  sepsis,  
thus  continuing  proteolysis.  
•   Liver  glycogenolysis  (16hrs)à  muscle  glycogenolysis  (24-­‐48  hrs)  
à  lipolysis  from  GI,  omentum,  heart  (7days)à  peripheral  :  
skeletal  and  intestinal  protiens  (3-­‐5days)  à  structural  and  
elemental  proteins  (heart,  kidneys)  (14-­‐21  days).  
•   Summary:    
o   30%  reduction  in  BEE  
o   Change  in  type  of  fuel  consumed:  fat  usage  
o   Change  in  type  of  fuel  consumed  
o   Relative  sparing  of  protein  
o   T3  decreases  
3.  What  conditions  contribute  to  malnutrition  in  surgical  
patient?  Pre  op,  Intra  op,  Post  op.  
ü    Preoperative  
o   Impaired  intake:  anorexia,  dysphagia,  sedation,  coma,  
poverty,  NPO  hours,  poor  food  service  in  hospitals,  
missing  meals  for  investigations,    
o   Impaired  digestion  and  absorption:  malabsorption  
o   Altered  metabolic  nutrient  requirements;  and  
§   Sepsis,  surgery,  burn,  malignancy,  chronic  infections  

 
 
 o    Excess  nutrient  losses  :  vomiting,  diarrhea,  3rd  space  
losses,  bowel  preparation,  high  output  stoma  
o   Underlying  malnutrition  
 
ü  Intra  op  
o   Bleeding  
o   Extent  of  resection  
o   Type  of  surgery:  e.g.  stoma  
§   0.5kg/day  for  6  days  because  of  the  response  to  
trauma  
ü  Post  op  
o   Period  of  NPO  
o   Complications:  SSI,  leak,  relap,  fever….  
o   Stomas  hyperfunctioning  
o   Immobilization    
o   Effects  of  RX:  chemoRx,  Radiation,  nausea,  vomiting  
4.  How  do  you  assess  nutritional  status  of  a  patient?  
ü  Anthropometric    
o   BMI:  BMI  >  30  or  <18.5  are  associated  with  
increased  postoperative  complications    
o   MUAC:  Indicates  acute  adult  malnutrition  
§   <18.5cm  -­‐  moderate  malnutrition  
§   <16  cm  -­‐  severe  malnutrition  
o   Triceps  skin  fold  thickness  
o   Ideal  body  wt.  
o   Usual  body  Wt  
o   DEXA  
ü  Biochemical  

 
 
 o   Serum  proteins  
§   ALBUMIN:  t1/2  =  18-­‐21  days  
•   Low  levels  correlate  with  chronic  
malnutrition  
•   Below  3  g/dL-­‐increased  risk  of  developing  
serious  complications  within  30  days  of  
surgery  
•   Cut  off  pts  
o   GI  surgery  -­‐-­‐-­‐  2gm/dl  
o   Colectomy  –  2.5  
o   Gastrectomy,  pancreatectomy  –  3.25  
o   Esophagectomy  –  3.75  
§   PRE  ALBUMIN/  TRANSTHYRETIN  
o   t1/2:  2.4  -­‐  3  days  
o   Most  useful  parameter  for  detecting  short-­‐
term  effects  of  nutritional  changes  
o    Reflective  of  nutritional  changes  within  3  
days  of  altered  nutrient  intake  
§   TRANSFERRIN  
o   t1/2:  10  -­‐12  days  
o   Reflective  of  acute  protein  deficiency  
o   Prognostic  indicator  of  mortality  &  
morbidity.  
o   Total  urinary  nitrogen  
o   Hematocrit  
o   Urinalysis:  protein,  sugar  electrolyte  loss  
o   FBS/RBS  
o   BUN  

 
 
 o   Globulins  
o   Liver  function  tests  
o   Serum  Lipids  
o   Total  lymphocytic  count  
o   Skin  tests  for  hypersensitivity  reactions  
ü  Clinical  
o   History    
§   Focused  assessment  of  risk  of  malabsorption  or  
inadequate  dietary  intake  
§    Dietary    →  anorexia,  food  intolerance,  
drug/alcohol  abuse  ,recent  wt  loss,    
§    Social    →    income,  living  situation  
§    Surgical/Medical    →    surgical  procedures,  chronic  
diseases  
§   Alimentary    →  
•   Abdominal  pain,  nausea,  vomiting  
•   Changes  in  bowel  pattern  
•   Difficulty  of  swallowing    
•   Early  satiety  
•   Indigestion  or  heartburn  
•   Pain  in  swallowing  

o   PHYSICAL  EXAM  
o   General  appearance→    wasted,  Loss  of  subcutaneous  
tissue  obesity  
o   Head  and  neck  exam:  Hair  loss,  bitemporal  wasting,  
conjunctival  pallor,  xerosis,  glossitis,  angular  cheilosis  
or  stomatitis.  

 
 
 o    Skin/mucus  membranes    →    decubitus  ulcers,  poor  
skin  turgor,  dermatitis,  ecchymoses,  petechiae,  pallor,  
pressure  ulcers,    signs  of  wound  infection    
o    Musculoskeletal    →    muscle  atrophy,  Edema    
o    Neurologic    →    Evidence  of  peripheral  neuropathy,  
reflexes,  tetany,  mental  status  ataxia,  night  blindness,  
encephalopathy    
 

ü  Dietary    
o   Detailed  dietary  History  /    
§   Usual  intake  of  food,  type,  amount  
o   24  hr  recall  of  actual  intake  
o   Food  frequency  questionnaire  
o   Weighted  or  measured  food  intake  
ü  Economic  
o   Socioeconomic  status  
o   Cultural  practices,  food  habits  
o   Food  prices  
o   Literacy    
5.  List  indications  to  nutritional  support.  
 
Diminished  food  intake  
Chronic  disease  
Diminished  digestion  and  absorption  
Hyper-­‐catabolic  states  
 
 
 
  Indications  for  perioperative  nutritional  support  
•   Severe  undernutrition  
•   BMI<18.5  kg/m2    
•   MUAC<170mm,  
•   Albumin  <3g/dl,  
•   Weight  loss  >10%  within  6  months  or  >5%  in  1      month)  
unintentional  
•    Failure  to  thrive  on  pediatric  growth  and  development  curves  
(<5th  percentile  or  a  trend  line  crossing  two  major  percentile  
lines)  
•    Anticipate  that  patient  will  be  unable  to  meet  caloric  
requirements  within  7-­‐10  days  perioperatively.  
•    Catabolic  disease  (e.g.,  significant  burns,  polytrauma,  severe  
sepsis)  
 
6.  Discuss  modes  of  nutritional  supplementation  including  
their  advantages  and  disadvantages?  
MODES  
1.  Enteral:  Nasogastric,  Nasoenteric  ,Gastrostomy,  
Jejunostomy    
Advantages  
o   Low  cost  
o   Risks  associated  with  IV  route  decreased  
o   Disuse  of  GI  leads  to  decreased  IgA  and  cytokine  
production,  bacterial  overgrowth  and  altered  mucosal  
defenses  

 
 
 o   44%  reduction  in  infectious  complication  in  critically  ill  
patients  
o   In  critically  ill  patients,  early  enteral  nutrition  is  
associated  with  
o   Better  small-­‐intestinal  carbohydrate  absorption,    
o   Shorter  duration  of  mechanical  ventilation,  and    
o   Shorter  time  in  the  intensive  care  
o   Often  well  tolerated  even  in  severe  illnesses  
Contraindications  to  enteral  nutrition  

o   Intractable  vomiting,  diarrhea  refractory  to  medical  

management  
o   Paralytic  ileus  
o   Distal  high-­‐output  intestinal  fistulas  (too  distal  to  bypass  with  
feeding  tube)  
o   GI  obstruction,  ischemia  
o   Severe  shock  or  hemodynamically  instability  
o   Severe  short  bowel  syndrome  (less  than  100  cm  of  small  bowel  
remaining)  
o   Severe  GI  malabsorption  (e.g.,  enteral  nutrition  failed,  as  
evidenced  by  progressive  deterioration  in  nutritional  status)  
o   Inability  to  gain  access  to  GI  tract  
o   Need  is  expected  for  <7  days    
 
  Complications  of  Enteral  feeding  
  Mechanical  
  Nausea  and  vomiting,  epistaxis,  sinusitis,  nasal  necrosis,  
  Aspiration  leading  to  pneumonia  

 
 
   Tube  malpositioning,  dislodgment  
  Rapid  administration  of  hyperosmolar  solutions    
  diarrhea,  dehydration,  
  electrolyte  imbalance,  hyperglycemia,  and    
  loss  of  K+,  Mg  ,  and  other  ions  through  diarrhea  
  Perforation,  stricture  
 
2.  Parenteral  
Indications  
o   Contraindications  to  EN  are  present  
o   Enteral  feeding  is  poorly  tolerated  
o   Limitation  of  GI  tract  function  

Complications  
1.  Technique  associated  complications    
  Sepsis  secondary  to  contamination  of  the  central  venous  
catheter  
  Pneumothorax,  hemothorax  
  Damage  to  vessels  (SCA  ,  Thoracic  duct  injury)    
  Air  embolism,  and  thrombosis  
2.  Overfeeding  complications    
3.  Intestinal  atrophy  
4.  Metabolic  complications  
o   Hypoglycemia  or  Hyperglycemia  
o   Hypertriglyceridemia  (acceptable  concentrations  <400  
mg/dl)  
o   Essential  fatty  acid  deficiency  
o   Azotemia  

 
 
 o   Metabolic  bone  disease  (osteoporosis  in  41%  of  those  on  
long-­‐  term  home  Pn)  
o   Elevated  liver  function  parameters  (increased  transaminase,  
bilirubin,  ALP  levels)  
 
 
3.  Mixed  
 
7.  List  Consequences  of  overfeeding  and  underfeeding.  
o   Overfeeding    
o   increased  oxygen  consumption,      
o   suppression  of  leukocyte  function,    
o   increased  risk  of  infection  Hyperglycemia  
o   Hepatic  dysfunction  from  fatty  infiltration  
o   Respiratory  acidosis  from  increased  CO2  production  
o   Difficulty  weaning  from  the  ventilator  
o   Risks  associated  with  under-­‐feeding:  
o   Depressed  ventilatory  drive  
o   Decreased  respiratory  muscle  function  
o   Impaired  immune  function  
o   Increased  infection