Eagle - Dr. Moataz 602.pdf

General Surgery Physio-chemical Introduction Atom: It is made of; 1. Nucleus: It contains a) Positrons or Protons: positively charged particles. b) Neutrons: neutral particles. The total number of both particles = (Atomic weight). 2. Electrons: - Negatively charged particles - Present in orbits...

General Surgery Physio-chemical Introduction Atom: It is made of; 1. Nucleus: It contains a) Positrons or Protons: positively charged particles. b) Neutrons: neutral particles. The total number of both particles = (Atomic weight). 2. Electrons: - Negatively charged particles - Present in orbits surrounding the nucleus. - Determine the chemical behavior of the atom - Are equal in number to the positrons. - They determine the (Atomic number ). Stable atom - The atom is stable when the force among the particles that make up the nucleus are balanced (their outer most energy level is full). - It needs at least 2 positrons in the nucleus and 2 electrons in the inner orbit. - The rest of the electrons are arranged in outer orbits. 1 General Surgery - Example of stable atom: Helium Atom o Atomic wight= 4 o Atomic number = 2 o N.B: The 1st energy level can antagonize the power of the 2 positrons. Unstable atom - It called Radio-nuclides (Radio-active). - Atom become unstable when the force among the particles that make up the nucleus are unbalanced. - So, the nucleus has an excess internal energy. - N.B: may result from excess neutrons, or protons. - Examples: Oxygen Atom o Atomic weight = 16 o Atomic number = 8 o Needs 2 more electrons to stability. o So, units with 2 H  H2O. 2 General Surgery - Hydrogen Atom o Unstable o Atomic weight = 1 o Atomic number = 1 o Lacks another electron o So, presents as H2. - Sodium Atom: o Unstable o A.W = 23 o A.N = 11 - Chlorine Atom: o Unstable o A.W = 35, 36 (35.5). o A.N = 17 3 General Surgery Isotope - An Atom can be bombed by neutron to form an isotope. - The atomic weight will increase, but the atomic number is still the same - So, the internal repel power will increase, the atom become radioactive. - Example: o Hydrogen o Deuterium o Tritium Heavy water - Deuterium, or Tritium can units with O2 to form a heavy water. - Which, can emit radiation. 4 General Surgery Introduction Electrolytes as ion: - Ions are electrically charged particles; may be either o Cations positively charged. o Anions negatively charged. - They may be either: o Atoms e.g. Na+ or Cl- o Large radicles e.g. HCO3- ,PO4---, …. o Molecules e.g. proteins (carry –ve charges at the pH of body fluids). Osmotic Activity of Electrolytes in Solution - The osmotic activity of electrolytes depends on the number of particles present i.e. ions. - Thus o 58.5 mg NaCl in one litre of water becomes:  23mg of Na+  one millimole/liter (mmol/l).  35.5mg of Cl-  one milimole/liter (mmol/l).  But the osmotic activity of the solution is 2 milliosmoles/litre (mosml/l). o 111mg of CaCl2 in a litre of water becomes:  40mg of Ca++  1 mmol/l  71mg of Cl-  2 mmol/l  Osmotic activity of the solution is 3 mosml/l. - Total Osmotic Activity of Plasma o Normally= 300 mOsm/l. o Na+ (140) + Cl- (100) =predominant contributors followed by HCO3- (27) and K+ (5), urea (5) and glucose (5) . - The osmotic pressure of the interstitial fluid differs from that of the plasma by 1.5 mOsm / l water (provided by plasma proteins) = a hydrostatic pressure of about 25mmHg. - Osmotic pressure of I.C. fluid is equal to that of the interstitial fluid: the main solutes are K+, Mg++, Protein and organic Po4--. 5 General Surgery - The difference in ionic pattern between the I.C. and E.C. fluid is due to the existence of a pump system. The cells actively extrude Na+ and then K+ passes inside the cells passively. The aim= to prevent the progressive diffusion of Na+ and Cl-. Composition of plasma Cations conc. mEq/l Na+ Anions conc. mEq/l 140 Cl- 103 K+ 5 HCO3- 27 Ionized Ca++ 3 HPO4--& SO4--&organic acid 8 Ionized Mg++ 1.5 proteins 16 Total ~150 Total ~150 Anion Gap - Difference between the sum of the concentrations of the major plasma cations and the major anions o =(Na+ & K+) - (Cl- & HCO3-) = 16 mmol/l or mEq/l o Raised level = due to ↑of other anions e.g. SO4--, PO4--, Lactate,hydroxybutyrate and acetoacetate.  Renal failure.  Lactic acidosis:   Inadequate tissue perfusion  Hypovolaemic shock  Septic shock) Diabetic ketosis o Low anion gap  not common & occurs in hypoalbuminaemia. 6 General Surgery Equivalent Atoms & Ions - The equivalent wt. is the amount in gm which unites or displaces one gm of hydrogen. - = Atomic weight or molecular weight in grams divided by its valency. - mEq or mmol = 1/1000 of the equivalent weight or molar weight o e.g. mEq of Na+ =23mg - o mEq of Cl- =35.5mg o mEq of Ca++ =20mg (Divalent-Atomic wt 40) Why we use mEquivalent Wt.: o Because the biological effect of electrolytes depends on its equivalent concentration i.e. the number of particles present and the number of charges carried on them. Reaction of fluids - Depends on the relative number of H + ions and OH- ions; o If more H + ions the reaction is acidic. o If more OH- ions the reaction is alkaline. - In pure water (H2O)  H + + OH- o The number of H + and OH-ions are equal, therefore pure water is neutral. H+ ions concentration in water - It is expressed as gm equivalent of ionic H + per litre of pure water at 22 °C and written as [ H+ ]=10 ‫־‬7 gm /L - In all aqueous solutions whatever the reaction, the product of [H +] and [OH-] is constant. o [H +]×[OH ‫ ═ ] ־‬10 ‫־‬7 x 10 ‫־‬7 ═ 10 ‫־‬14 o If [H +] is 10 ‫־‬6 the [OH-] is 10 ‫־‬8 and the solution is acidic o To avoid the negative indices, we use the pH.  pH = - Log [H +]  A solution of pH  If pH exceeds 7 alkaline  If pH is less than 7 acid 7  neutral 7 General Surgery Acids and Bases - An acid is a molecule which is capable of yielding H + ions. - A base is a molecule or ion which is capable of taking up H + ion to form an acid. o A strong acid readily gives up its H +, while its conjugate base less readily accepts this H +. e.g: HCl (a strong acid) H + + ClH2CO3 (a weak acid) H + + HCO3- (a weak base) (a strong base) o N.B. cations like Na+ and K+ were once called fixed bases. They are neither acids or alkalies. Buffers - A buffer is a substance capable of mopping up an excess of H+ ions and also able to contribute H+ ions if the pH rises too much. - It consists of a strong base and a weak acid e.g. HB (weak acid)  H + - + B- (strong base) If there are excess H+ ions, they will combine with B- (the strong base) to form weak acid. - If the pH rises there is increased dissociation of the acid to provide more H+ ions. - The ideal buffer is: H2CO3 8 General Surgery Water Metabolism Physiological considerations: (I) Amount: - An adult male, 70 kg has 60% of his body weight water = 42 liters, - An adult Female has 55% of body weight (due to more fat contain) - A new-bon has 75% of body weight. (II) Distribution: divided as: 1- Intracellular (2/3) = 28-30 L. 2- Extra-cellular (1/3) = 12-14 L - Interstitial (3/4) = 9 - 10.5L. - Intravascular (plasma) (1/4) = 3 - 3.5L. - Trans cellular (1.6%) = fluids in the G.I.T., C.S.F, and aqueous humor. (III) Water distributes freely: through all the above mentioned compartments to bring the osmolarity of all compartments into equilibrium. Factors control this equilibrium are : 1- Capillary membrane (endothelium): allows the passage of water and electrolytes (but not proteins - colloids) except for a small quantity of plasma albumin cross to the interstitial compartments controlled by, starling forces, which are : a. Colloid pressure of plasma proteins : (25mmHg) draw fluid into the capillaries. b. Hydrostatic pressure: push fluid out of the capillary to interstitial compartment. 2- The cell membrane : • The barrier between the extra and intracellular space. • It's freely permeable to water, but not to Na+ which actively pumped out of cells. • So, Na+ is mainly an Extra cellular cation. Kf is mainly an Intracellular. • Both cations control the osmolarity across the cell membrane, and hence control water shift between the 2 spaces. • Since each cation is balanced by an Anion so, osmolarity of plasma (intravascular) or ECF (extra vascular) is calculated from: Osmolalilty (mOsmol/kg) = 2(Na+ +K+) + glucose + urea level (mmoI/L) 9 General Surgery (IV) Normal water balance : • Water input = Exogenous (Drink 1500, food 1000). Endogenous (Metabolic water) 300-500 cc/dy. • Water output : 1. In the urine: (1500/day) - The minimal volume of urine enable the kidneys to excrete waste products is 400 ml = volume obligatore. 2. Unavoidable or Insensible Water loss: A) Perspiration through the skin  600:800ml per 24 hours. B) Respiratory loss 400 ml per 24 hours. C) In the faces~ 100 ml per 24 hours. 3. Sweat: variable depend on the temperature of body or environment) (V) Water Regulation: - Insensible water loss is necessary for regulation of body temperature. - The kidneys are the only organs that regulate water loss. a. About 170 liters of water are filtered by the kidneys every day. b. 80% of this volume is reabsorbed in the proximal tubules secondary to absorption of glucose and salt = Obligatory water absorption. c. 20% =35 liters are reabsorbed in the distal tubules except for the amount passed as urine =1500 ml. - In cases of hydration  more dilute urine is excreted and in dehydration small volume of concentrated urine is excreted. This is under control of 2 hormones: 1. ADH: - Secreted by the posterior pituitary under the influence of nervous impulses originating in the supraoptic nucleus of the hypothalamus. - This is stimulated by osmoreceptors which are sensitive to changes in the osmotic pressure of plasma crystalloids. - If the plasma diluted  inhibitition of ADH production diuresis and vice versa. 2. Aldosterone : absorb water through augmenting the reabsorption of sodium. 10 General Surgery Water Depletion = (Pure Dehydration) Causes : 1- Lack of intake :  availability, difficult to swallow or comatosed. 2- Diabetes insipidus. 3- Unreplaced losses : as losses from lungs after tracheostomy. 4- Increased output: as in fever and osmotic diuretics. Water deficit →  volume in all body compartments → hyperosmolarity (as no change in solute) → stimulation of osmoreceptors → ↑ ADH → increase water resorption from kidney, for correction. Clinical Picture: 1- Intense thirst and weakness. 2- Decreased tissue turgor. 3- Oliguria + high specific gravity of urine. Management: A) Estimate the deficit: (each 3mEq elevation of serum Na+ concentration above normal range = 1 liter deficit of body water). B) Treatment: 1. Mild depletion, conscious patient: water by mouth. 2. If severe depletion, 1/2 the estimated deficit should be replaced in the 1st 12 hours, as rapid changes in osmolarity may result in neurological changes. 3. Replaced by I.V glucose 5%. the glucose make the solution isotonic to (ECF). 11 General Surgery Water Excess (water intoxication) Causes : 1- Excessive administration of water to sodium-depleted patients. 2- Over infusion of 5% glucose I.V to postoperative patients. 3- Colorectal washout by water enema instead of saline before colonic surgery. 4- T.U.R. syndrome after transurethral removal of the prostate.. 5- Neurosis (excessive intake). - Neurosis (excessive intake). Water excess →  volume of all fluid compartments → hypo-osmolality (as solute contents of body can't be altered) → osmoreceptors → ADH →  renal water excretion. Clinical Picture ; A) Moderate water excess → well tolerated → minimal symptoms : 1.  urine volume. 2.  body weight. 3.  serum Na+ concentration and  hematocrite. B) Marked water excess → (only if serum Na+ cone. < 120 mEq/L) 1. Brain oedema → drowsiness, weakness and finally convulsions and coma. 2. Nausea and vomiting of clear fluid. Management: 1. Mild cases → only restrict water intake. 2. Severe cases → forced diuresis by mannitol. 3. If renal failure → dialysis is required. 4. If convulsions → 100-250cc I.V. 5% sodium chloride solution. 12 General Surgery Electrolyte Metabolism Dissolved in the body water are different inorganic salts that are dissociated to positively charged Cations and negatively changed Anions.  Under normal conditions, the number of Cations (Na+, K+) must equal the number of Anions (CL, HCO3 , Phosphate sulphate, proteins and organic acids). The level of cations and anions in ECF: MmoL/L Cations Anions Mmol/L Na+ 140 CL 105 K+ 5 HCO3- 25 Total 145 Total 130 N.B.: The difference in the total due to unestimated small fraction of phosphate, sulphate ...etc. The chemical composition of body secretion: 13 General Surgery Sodium Physiological consideration : • Main extra cellular cation, - Controlling blood volume and plasma osmolality. - Essential for the renal function. • Total body Na is 5000 mmol = ECF 44%, ICF 9%, Bone 47% (Na+ store house of body) • The average daily intake = 1 mmoL/kg. equivalent to 500 ml of 0.9% normal saline. • Obligatory  Na+ excretion (Na+ excretion shut down) follows surgery or trauma for 48 hours due to  aldosterone.(Conservative method) (I) Pure hyponatremia (2ry dehydration) - Uncommon. - Considered as water intoxication. (II) Hyponatremia (Sodium & Water Deficiency Causes: 1) Abnormal GIT loss: vomiting, diarrhea, gastro-intestinal fistulae. 2) ECF loss: burns, marked sweating, 3) Excessive sodium loss in urine (diuretics, salt losing nephropathy). 4) Hypovolaemia and adrenocortical insufficiency. 5) Restricted dietary intake. Clinical Picture: (decreased ECF volume) 1. Sunken eyes and depressed fontanels in infants. 2. Dry coated tongue. 3. Dry wrinkled skin + lax subcutaneous tissues. 4. Collapsed skin veins. 5. Hypovolaemia: Tachycardia + orthostatic hypotension and shock.. 6. C.V.P. + oliguria. 7. NOooo THIRST. 14 General Surgery Treatment: I) Replace pre-existing loss (pre-operative replacement): - Replacement by normal saline (NaCL 0.9%) or Ringer's lactate (sodium chloride + K+ + Lactate). II) Once replacement occurred, treat the cause, (e.g pyloric stenosis). Replace observed loss (if no operation needed): - Replace by saline. - More than 2 days or 2 liter loss, think about K. - In acidosis, replace by 1/6 Na lactate. (III) Hypernatraemia Causes: 1. Excessive saline transfusion in the early postoperative period. 2.  Na+ re-absorption ( aldosterone, cortisone or estrogen). 3. Inability to excrete sodium load (severe illness or starvation). 4. Abnormal renal retention of sodium (renal, heart and liver failure). Clinical picture: 1. Slight puffiness of the face is the only early sign. 2. Total body oedema. 3. Weight gain. 4. Hypertension and Ascites. Treatment: 1. Sodium restriction 2. Careful use of diuretics (I.V frusemide ). 3. Inotropics. 4. If oedema + hypoproteinaemia → protein deficit must be corrected first . 15 General Surgery Potassium Physiological considerations: • K+ is the main intracellular cation. • 75% of the total body K+ is found in skeletal muscles. • The normal daily intake = 1 mmol/Kg. - Essential for excitability of nerve, and muscle. - Essential for the action of the heart. - Regulation: o Depends on the intake. o Excreted in urine. o No conservative procedure. • Factors affecting K+ distribution : 1. Acid-base : - Acidosis → Hyperkalemia, - Alkalosis → hypokalemia. 2. Insulin : Stimulates intracellular K+ shift. 3. Excessive cellular breakdown :  plasma K+ concentration . 4. Osmolality : Hyperosmolarity → K+ concentration in plasma. 5. Exercise :  plasma K+ concentration. (I) Hypokalaemia Causes : 1. Decrease the intake. 2. Vomiting (e.g. pyloric obstruction), prolonged gastro-duodenal suction. 3. External gastrointestinal fistulae. 4. Severe diarrhea (ulcerative colitis, villous rectal tumours). 5. K+ losing diuretics (e.g. furosemide). 6. Alkalosis : due to shift of K+ into the cells. 7. Hormones : insulin and steroids. 16 General Surgery Hazards of hypokalemia : 1.  nerve and muscle excitability. 2.  risk of supra-ventricular arrhythmias in patients taking digitalis. 3.  risk of hepatic coma in hepatic patients. 4. Polyuria due to responsiveness to ADH. Clinical Picture : 1. Early signs: vague, malaise and weakness. 2. Paralytic ileus and distention 3. Cardiac arrhythmias. 3. Muscular paresis (with extreme depletion). 4. ECG reveals: prolonged QT interval, depressed ST segment and inversion of "T" wave, prominent U (biphasic). Management: - Estimation of K+ deficit: from the total body K+ capacity, ABG and serum K level. - K+ can be very dangerous, as hyperkalaemia causes cardiac arrhythmias. - It should never by injected as a bolus, but slow I.V infusion with the following safe rules: - Correct first salt and water deficiency. - Urine output at least 40ml/hour. - No more than 40 mEq (mmol) added to 1 liter fluid. - No faster infusion than 40 mmoL/hour. - Not more than 100 mEq/day. - K should be estimated dialy. - Once, the patient can swallow, shift to oral replacement. Potassium solutions used: 1. 2. Potassium is available in small bottles containing 10% solution of KCl.  30ml of this solution is added to one litre of glucose 5% or saline.  This provides a solution of 40mEq of K+. Darrow's solution; Each litre contains 124 mEq Na+ 36 mEq K+ 104 mEq Cl- 56 mEq lactate. 17 General Surgery (II) Hyperkalemia Causes: 1. Renal failure. 2. Acidosis. 3. Diabetics with reduced insulin secretion. Clinical picture: 1. ↑ Cell excitability (muscles & nerves). 2. Cardiac arrhythmias, Bradycardia, hypotension and finally arrest. 3. ECG : shows wide QRS complex and peaked T wave. Treatment: 1. I. V. calcium gluconate as calcium antagonizes K+. 2. I.V. NaHCO3 → alkalosis→ intracellular K+ shift. 3. 20gm glucose + 10 units regular insulin infusion (glucose is given to prevent hypoglycemia). 4. If the previous measures fail (> 6 mmol/l) → ion exchange resins 50gm in 70% sorbitol by mouth or enema. 5. If all the previous measures fail (> 7 mmol/l) → dialysis should be started. Calcium It is an extracellular cation, its plasma concentration is 4.5: 5.5 mEq/l. Calcium exists in 3 forms: 1. Free ionized: it is the most active 2. Free non-ionized. 3. Bound to protein.  Free ionized Ca++ in blood: its level is 2.3:2.6 mEq/l.  It is necessary for blood coagulation and neuromuscular excitability.  Its level falls in (alkalosis) causing tetany.  In the urine, also the ionization and solubility of Ca++ diminishes if pH rises and this may predispose to stone formation. 18 General Surgery Factors affecting Blood Ca++ level 1. Parathormone: a) mobilize Ca from bones hypercalcaemia. b) increases its excretion by the kidneys. 2. Calcitonin: help storage of Ca++ in bones  hypocalcaemia. 3. Vitamin D: it increases its absorption from the bowels hypercalcaemia 4. Phytic acid: it inhibits its absorption from the bowel  hypocalcaemia Hypercalcaemia: It is usually due to a parathyroid tumour which has to be removed. Hypocalcaemia: It is seen in: 1. Hypoparathyroidism as a complication of thyroidectomy. 2. After massive blood transfusion containing CPDA (Citrate Phosphate Dextrose Acid). Treatment 1. 10 ml of 10% Ca gluconate I.V: emergency measure. 2. Long term treatment: - Calcium by mouth - Vitamin D. Magnesium Mg++ is an intracellular cation. Its concentration in the plasma is 1.8:2.2 mEq/L. Its ionized part is 0.7: 0.9 mmol/L. Magnesium Deficiency: It occurs in prolonged GI losses, cirrhosis and prolonged I.V. fluid therapy or I.V. hyperalimentation (TPN). Clinical Picture: 1. 2. Diagnosis: CNS irritability. Hypotension. Measurement of urinary Mg++ after an IV loading dose. Normally 90% is excreted in the urine. Treatment: 1. 2. Mg++ can be given IV as Mg sulphate 80 mEq/l In TPN it is necessary to give Mg++ supplements. 19 General Surgery Acid-base disturbance Physiological consideration: • An acid = is a hydrogen ion (H+) donor. • A base = accepts hydrogen ion. • Body produces (H+) and they must be either excreted or buffered to keep the PH of internal environment constant at a range of (7.3 - 7.5). • Mechanisms of PH regulations: (How blood reaction is regulated) I) Physico-Chemical (Body buffer systems) : - Consists of weak acids and strong bases, - Divided into: a) Extracellular buffers. -H2CO3: BHCO3 -NaH2PO4: Na2HPO4 -Plasma Proteins (Proteinic acid : Na Proteinate) b) Intracellular buffers. -Hb system in RBCS. -Tissue buffers (tissue protein, phosphates& bicarbonates). - Most important is bicarbonate : carbonic acid ratio which is normally 20: 1 - Alteration in this ratio changes the PH, regardless of the absolute value of bicarbonate and carbonic acid, alteration of one is followed automatically by a compensatory change by the other, so that the ratio remains constant). - Example: when lactic acid is added to the circulation: Lactic acid + NaHCO3  Na lactate + H2CO3 H2CO3 is less strong than lactic acid and can be excreted through the lungs. 20 General Surgery II) Next by: Physiological Regulation: A)Respiration:  If Acidosis, respiratory centre is stimulated directly through chemoreceptors.  Respiratory movements will increase in depth and rate.  This helps in liberation of excess CO2 and diminishes the H2CO3 in the same proportion of HCO3 so that there is no change in the pH.  IF Alkalosis, the respiratory centre becomes depressed. The CO2 tension in the alveoli rises and the ↑H2CO3 in the blood rises to keep the ratio BHCO3/HHCO3 = constant. CO2 + H2O H2CO3 H + + HCO3 B) Kidneys 1) Phosphate mechanism  The ratio of Na H2 PO4 : Na 2H PO4  In the plasma is 1:4 .  In the glomerular filterate is 1:4 .  In the urine is 9:1.  In acidosis all phosphates are excreted in the acid form and so spares Na+, And in alkalosis more of the basic salt is excreted. 2) Ammonia mechanism - Renal tubules can manufacture NH3 from amino-acids - To neutralize acid substances. - As a result: ammonium salts are formed and the spared Na+ is reabsorbed. This mechanism is very active in ketosis e.g. Na aceto.acetate + NH3  Ammonium aceto.acetate + Na - In alkalosis the mechanism is depressed. 3) Direct excretion by the Kidneys in the urine. 1. Bicarbonate in alkalosis. 21 2. Ketoacids in acidosis. General Surgery (I) Metabolic Acidosis Definition: It is a base deficit or acid excess other than carbonic acid. Causes: 1. Overproduction of an organic acid which occurs in : a. Diabetic ketoacidosis. b. Lactic acidosis of anaerobic sepsis, shock, ischaemia. c. Salicylate toxicity or hyperalemintation due to excess amino acids. 2. Impaired renal excretory mechanisms in : a. Acute and chronic renal failure, b. Renal tubular acidosis. 3. Abnormal loss of bicarbonate in : a. Diarrhea, pancreatic or small intestinal fistulae. b. Uretero-sigmoid anastomosis after removal of the urinary bladder. c. Diamox (Acetazolamide) therapy. Pathophysiology : • Metabolic acidosis is partially compensated by stimulation of respiratory activity ( rate and depth of respiration) → washing out CO2 →  PCO2 → bringing bicarbonate / PCO2 and PH to normal (the standard bicarbonate level is lowered due to  CO2 wash and there is a BASE DEFICIT) • In patients with chronic pulmonary disease, renal correction of acidosis occurs by  renal excretion of H+ ions→ strongly acidic urine Treatment 1) Mild to moderate acidosis → treat the underlying cause. 2) Server acidosis (PH<7.3, serum bicarbonate=15 mEq/L) give I.V bicarbonate estimated as : Body weight (kg) x 0.3 x base deficit 22 General Surgery (II) Metabolic Alkalosis Means rise in the pH due to accumulation of bicarbonate, It can be produced either by: a. Retention of bicarbonate. b. Loss of H+ through G.I.T. or urine. > The acid lost is produced from intracellular dissociation of carbonic acid (H2CO3). CO2 + H2O  H2 CO3  H + HCO > For each H+ lost, an equivalent amount of bicarbonate is generated. Metabolic alkalosis is therefore a condition of base excess or acid deficit. Causes: 1. G.I.T. \ Excessive vomiting or suction of gastric secretion 2. Renal losses of H+ :  Aldosterone, Hypoparathyroidism. 3. Hypokalaemia : stimulates intracellular H1 shift. 4. Bicarbonate retention : Milk alkali syndrome. 5.  plasma bicarbonate with severe  ECF (e.g. severe vomiting), the extracellular space contract over a constant amount of bicarbonate → relative  in bicarbonate level. Clinical Picture : 1) Cheyne-stokes respiration (slow and deep) with periods of apnea. 2) Tetany ( level of ionized Calcium). 3) Hypokalaemia. Management: 1) I.V saline infusion: is sufficient in mild metabolic alkalosis without hypokalemia (kidney will correct by retaining CL and excreting Na+ along with excess bicarbonate). 2) If hypokalemia : (from excess K+ loss in urine in exchange for Na+ and H+ ions to compensate alkalosis) → give I.V potassium chloride. 3) If severe alkalosis not responding to the above measures give : a. Ammonium chloride slowly I.V. b. I.V hydrogen chloride through central line given.. 4) If tetany → gives l0 cc of 10% calcium gluconate I.V. slowly. 23 General Surgery (Ill) Respiratory Acidosis Fall in pH associated with a rise in PCO2, it is always associate with hypoxia, and respiratory depression (CO2 narcosis), renal compensation is too slow to correct this life threatening condition. Causes: /) Respiratory depression by : • Drugs as opiates. • CNS lesions and cardiac arrest. 2) Disorders of respiratory muscles : • Myasthenia. • Flail chest. • Morbid obesity. • Pulmonary fibrosis. 3) Impaired alveolar function from : • Chronic obstructive pulmonary disease. • Pulmonary oedema. Clinical Picture: 1) The patient is restless and usually cyanosed. 2) Postoperative hypertension and tachycardia from inadequate ventilation and hyper capnea. 3) The diagnosis is best made by estimation of serum PH and PCO2, Serum HCO2 level may remains normal since renal compensation has not had enough time to act Treatment: Improving ventilation + aiding renal compensation 24 General Surgery (IV) Respiratory Alkalosis Causes: 1)Hyperventilation as seen in : • Hysteria, hyperpyrexia. • Bacterial sepsis. • Brain stem lesion. • Hyperventilation by ventilators. 2) Patients undergoing neurosurgical procedures may be hyperventilated to  cerebral blood flow. Clinical Picture : 1. Tetany in severe alkalosis. 2. Respiratory arrest. 3. Alkalosis of any degree may impair cardiac output in patients with cardiac disease Respiratory alkalosis is short lived and corrected when hyperventilation stops Treatment: 1. If hysteria → instruct the patient to breath into a bag. 2. Sometimes → CO2 addition to inspired gas mixture but the danger is in mistaking a compensatory metabolic acidosis. 25 General Surgery Diagnosis of acid base imbalances : PH PO2 PC02 HC03 Normal 7.36-7.44 80- HOmmHg 36-44mmHg 22-26mmol/l Metabolic Reduced Normal Reduced due to Reduced Deficit Elevated Excess Elevated due to Excess acidosis Metabolic resp. wash out Elevated Reduced alkalosis Respiratory Elevated due to resp. retention Reduced Reduced Elevated acidosis Respiratory Base renal retention Elevated Normal Reduced alkalosis Reduced due to Deficit real retention Postoperative fluid and electrolyte therapy: /- Points to be considered : * Base requirements. * Pre-excising dehydration, electrolytes or acid base imbalance. * Abnormal losses from fistulae, vomiting, or third space loss like peritonitis. //- Postoperative fluids for uncomplicated surgery in an adult: * 3 liters of fluids + 200 cc for each 1°C rise in temperature. * 500ml (0.9% saline) provides daily Na+ requirements. * 2.5 liters dextrose 5%. * K+ is given after 48 hours. Either dextrose is replaced by kadalex (27 mmol KVliter) or potassium chloride ampoules are added. Interpretation of ABG: 1- Is the patient is hypoxic (PO2< 75mmhg). 2-Is the patient Acidotic or Alkalotic? • PH < 7.38 = acidotic • PH > 7.42 = alkalotic. 3-Is primary disturbance Respiratory or Metabolic? Look for the PCO2 & serum HCO2 * Respiratory disturbance primarily alters the arterial PCO2. * Metabolic disturbance primarily alters the serum HCO2 26 General Surgery 27 General Surgery Hemorrhage Definition: Escape of RBCs outside the vessles, or organs Classification: Site 1. External: wounds or epistaxis or haematemesis. 2. Internal: a. In body cavities, e.g., haemoperitoneum and haemothorax. b. Interstitial, e.g., fracture haematoma. Type of vessel 1. Arterial. Blood is bright red and comes in pulsatile jets. 2. Venous. Blood is dark red and comes in a steady flow. 3. capillary. Bleeding occurs as diffuse ooze of bright red blood. Timing: 1. Primary haemorrhage occurs at the time of trauma. 2. Reactionary haemorrhage - Occurs within 24 hours after trauma . - Due to an insecure ligature slips or a clot is dislodged. 3. Secondary haemorrhage - 1- 2 weeks after trauma, due to infection eroding a vessel wall - It can be fatal if a large artery is involved. Aetiology 1. Traumatic  Accidental.  Surgical.  lnterventional procedures, e.g. percutaneous transhepatic cholangiography (PTC). 2. Pathological  Atherosclerotic (ruptured aortic aneurysm) .  Inflammatory (bleeding peptic ulcer).  Neoplastic (haematuria In renal cancer}. 3. Bleeding diathesis can increase the amount of traumatic and pathological bleeding, or cause bleeding with little or no trauma (spontaneous haemorrhage). 28 General Surgery Physiological response to hemorrhage: Locally: Stopping the bleeding - Vasoconstriction and retraction of the intima of the injured vessel. - Platelet plug. - Blood clotting. They are more effective when the vessel is completely transected than when there is a side tear, and in traumatic than in pathological cases. Systemically: A. Neural factors. ↓ stimulation of arterial baroreceptors (aortic arch and carotid sinus) and atrial stretch receptors → Inhibition of the normal inhibitory discharge in the vagus and glossopharyngeal nerves on the vasomotor centre  stimulation of the sympathetic system.  The effects include: 1. Constriction of veins: - Normally contain two-thirds of the blood volume - Displaces blood from the periphery into the heart. 2. Constriction of arterioles - Involves mainly the arterioles of the skin, skeletal muscle, and splanchnic area  Raises the peripheral resistance. 3. Increased rate and strength of cardiac contraction. Maintaining effective circulatory volume and perfusion of critical tissues (brain and heart). at the expense of less critical tissues (skin, skeletal muscle and splanchnic area). B. Endocrine factors 1 Catecholamine: ↑heart rate and myocardial contraction and cause constriction of them arterioles of the skin, kidney and viscera. 2 The metabolic hormones  ↑ACTH, cortisol, growth hormone and glucagon.  Insulin release is inhibited by adrenaline and noradrenaline. 29 General Surgery 3 The renin-angiotensin aldosterone system. - Renin secreted in response to renal hypoperfusion. - Renin splits angiotensinogen to angiotensin I - Which is converted to angiotensin II by a converting enzyme in the lung. - Angiotensin II is a powerful vasoconstrictor and sodium and water retention by the kidney as well as release of aldosterone. 4 ADH (vasopressin). C. Transcapillary refill.  ↓blood volume and constriction of arterioles  drops the capillary hydrostatic pressure and promotes movement of fluid from the interstitium into the capillaries.  The resulting haemodilution increases the blood volume and lowers its viscosity, thus improving effective circulatory volume. N.B - This Mechanism can compensate for losses up to 15% of blood volume only. - Blood volume is estimated as 70 ml/kg in adults, 80ml/kg in children. - i.e in adult : 15% from 5 Liters = 750 cc - in neonate: 10 % from 280 cc = 28 cc Clinical Picture Symptoms 1 Weakness and fainting especially when standing. 2 The patient feels cold and thirsty. Signs 1 Mental status: vary from anxious to drowsy.. 2 Pulse and blood Pressure. - Mild loss (< 500 ml): Pulse and B.P may remain normal. - More loss: Tachycardia but the blood pressure remains stable. - Further loss: Hypotension develops. 3 Respiratory rate· Tachypnea and air hunger. 4 Temperature.  Hypothermia 5 Skin: Pale, cold (vasoconstriction) and clammy with slow capillary refill. 6 Oliguria results due to diminished renal perfusion. 30 General Surgery Estimating blood loss  Blood volume is estimated as 70 mi/Kg in adults and 80 mi/Kg in children. 1. Clinical data Blood loss Mental status Skin Capillary refill Blood pressure -systolic -diastolic -pulse pressure Respiratory rate Urine (ml/h) 2. Class II 15-30% (750-1500 ml) Aggressive to-drowsy. Pale and cold <2 sec. Class III Class IV 30-40% <40% (1500-2000ml) (<2000ml) Anxious Drowsy restless. to unconscious Pale and colder. Pale and very cold <2 sec. <2 sec. undetectable. Normal Normal Normal 14-20 <30 Normal(supine) Raised Low 20-30 20-30 Low Low low 30-35 10-20 Low Low low <35 0-10 Type of injury.    3. Class I Up to 15% (750ml) Normal to anxious) Normal Normal Haematoma around a fracture of the tibia may contain 500-1500 ml of blood. Fractured shaft of femur, soo-2000 ml; Fractured pelvis, 2000-3000 mi. Blood loss at operation  Sum of the suction reservoir and the amount mopped up by the swabs. 31 General Surgery Management of Hemorrhage Stop hemorrhage.     (Packing, Pressure, Position) The wound is covered by a dressing And pressure is applied manually, or by a sphygmomanometer cuff. o Tourniquets are contraindicated. Elevation of the limb above the heart (decreases arterial bleeding). Other examples: o Anti-shock garment (PASG), o Balloon tamponade from oesophageal varices. Restore blood volume. Class II     The deficit is estimated at 15-30% {750-1500 ml/70 kg). The replacement solution is lactated Ringer's. The amount is 3 times the estimated deficit (3:1). Administration. o Two liters are given as a bolus. o If there is definite improvement: the remaining litre is given more slowly followed by the maintenance requirements and continued observations o Haematocrit <30 requires blood transfusion. o If there is moderate improvement. the possibilities are:  inadequate replacement.  Cardiac tamponade and tension pneumothorax.  Blood transfusion is started if bleeding is still active. Class III and IV     Management as class II till blood transfusion. Plasma expander can be used until blood is available. The volume of transfused blood equal the estimated deficit (1:1). Failure to improve and a rising OJP indicate: o Tension pneumothorax, Cardiac tamponade, Cardiac failure. o Major thoracic, abdominal, or pelvic injury. 32 General Surgery Optimize oxygen delivery.    40% oxygen is given for class II haemorrhage 100% for classes Ill and IY. Mechanical ventilation can be used to improve oxygen delivery. General care of the patient.   Bed rest and analgesia (morphia, 3-5 mg IV). Morphine: contraindicated in head injury and in respiratory insufficiency. Monitoring:      Foley's catheter. Vital signs. C.B.C: haematocrits ECG for early detection of shock-induced arrhythmias. Invasive Monitoring: - Central venous pressure - A pulmonary artery catheter Failure to respond to fluid resuscitation: CVP low= continuous bleeding. CVP high= tension pneumothorax -cardiac tamponade- cardiac contusion N.B Of Reactionary Hemorrhage: a. Resuscitation by fluids or blood transfusion. b. Secure legation or angiographic embolisation of the bleeding site. N.B Of secondary hemorrhage : a. Surgical legation of the bleeding vessel proximal to the eroded site. b. Or packing of the bleeding site if tissues are friable from infection which makes legation difficult + broad spectrum antibiotics. 33 General Surgery Shock Definition: A pathophysiologic condition that leads to inadequate tissue perfusion that results in impaired cellular metabolism. Aetiology/Classification : Adequate tissue perfusion depends on 3 factors : a. Blood volume, b. Capacity of the blood vessels, c. Pumping action of the heart. (1) Hypovolaemic shock : a. Loss of blood_→ hemorrhage (internal, external). b. Loss plasma→ burns. c. Loss of watery →severe vomiting & diarrhea. (2) Cardiogenic shock : a. Inefficient cardiac contraction → as in (myocardial infarction).. b. Cardiac filling → as in cardiac tamponade and pulmonary embolism. (3) Vasogenic shock : a. Septic shock : Vasoactive substances  impaired microcirculation. b. Neurogenic shock : loss of vasomotor tone due to sympathetic paralysis. c. Anaphylactic shock : severe VD + capillary permeability due to histaminc release from antigen-antibody reaction, d. Endocrine shock : in patient with acute adrenal insufficiency . 34 General Surgery Hypovolemic Shock Aetiology: Diminished blood volume:  Blood :As in internal or external hemorrhage.  Plasma :As in bums and peritonitis.  Fluids :As in severe vomiting, diarrhea & intestinal obstruction. Patho-physiology of Hypovolamic shock: - Reversible (compensated) Stage: (Physiological response to hemorrhage). - Irreversible (decompensated) Stage: Microirculatory changes: 1 Under the effect of catecholamines the precapillary sphincters constrict. 2 Hypovolemia → hypoxia → opening more capillaries. The results are:  Further slowing of capillary circulation  Extensive coagulation of blood in these capillaries → DIC. 3 A sluggish circulation & DIC →↑ tissue hypoxia  dysfunction of capillary endothelium.  This leads to leakage of large protein molecules from the vessels to the interstitial space dragging with them huge amounts of fluids (third space loss) with more profound hypovolaemia. Cellular Derangement: 1 Hypoxia  anaerobic glycolysis →↑ lactic acid  cellular functions.  Failure of Na/K pump  Na and water retension. 2 End in rupture of cell membranes and cell death. Acid-base imbalance: Metabolic Acidosis. Effect on organs: (MOSF) 1 The heart:  Impaired Myocardial contractility by tumor necrosis factor (TNF) (myocardial depressants). 2 Intestine:  Translocation of bacteria from the ischemic gut mucosa into the circulation → multiple organ system failure. (septic death) 3 Stomach: true stress ulcers. 4 The liver: ischemic Hepatic dysfunction is a frequent component of MOSF. 5 Renal affection:  Acute tubular necrosis  failure. 6 Pulmonary response: ARDS occur as part of MOSF. 35 General Surgery Clinical picture : see before Treatment 1. Stop the hemorrhage 2. Restore the blood volume: 3. Oxygen delivery: (As Hemorrhage) 4. General care: 5. Inotropic: (the 2nd line of treatment) - Dopamine & dobutamine improve myocardial contractility, - While dopamine improves renal blood flow. 6. Monitoring. - Clinically : Pulse, blood pressure, temperature, respiratory rate. - Foley's catheter: For urine output monitoring (0.5- 1 ml /kg/hour). - C.V.P.: - Normally (5-10 cm H2O). - Reflect the volume of blood returning to the right side of the heart and the ability of the heart to expel it. - Pulmonary artery wedge pressure: (PAWP) - Normally: (25 mmHg systole/10 mmHg diastole) - By the use of Swan Ganz catheter, In unstable cardiovascular patients. - To monitor right atrial pressure - Pulmonary capillary wedge pressure (PCWP) normal between 8 and 12 mmHg or 10-15cm of water. - Advantages of Swan-Ganz catheter:  Differentiate between right and left ventricular failure.  Accurate guide for I.V. fluid therapy, inotropic agents and vasodilators.  Measure cardiac output by a thermodilution technique.  Used to obtain samples of mixed venous blood for oxygen saturation. - ECG. : To detect any arrhythmias. - Hematocrit and Haemoglobin values - Blood Gases: - PO2: 80-100 mmhg - PCO2: 35-45 mmhg 36 General Surgery Septic Shock Definition:  The most serious type of shock and the most difficult to treat.  Considered as a part of SIRS {systemic inflammatory response syndrome) Etiology:     Resistant and virulent organisms. Concentration of infected patients in critical care units. Severely injured patients. Immunosuppressed (DM, transplantation, radiotherapy and chemotherapy). Predisposing factors : - Old age, diabetes mellitus, corticosteroids, chemotherapy & malignancy. Causative organisms : 1. Gram- ve bacilli {commonest). 2. Staphylococci. 3. Candida. Pathophysiology: 1. Mediators cascade: - Endotoxins of Gram -ve bacteria, stimulates macrophages, which in turn stimulates the production of large amounts of inflammatory mediators (cytokines) - Cytokines (harmful mediators) include: Tumor necrosis factor (TNF), interleukines, prostaglandins, nitric oxide, platelet activation factors. - N.B: IL-2, IL-10 (normal mediators) are limited. - Excess cytokines cause the following major problems: 1. Platelets and leucocytes adherence to the vascular endothelium: - Microvascular hypoperfusion. - Release of free oxygen radicals  damage vascular endothelium. 2. Damage of the Gut barrier  intestinal flora enter into the circulation. 3. Excessive Nitric oxide (by vascular endothelium) which is a potent smooth muscle relaxant leading to the decreased peripheral resistance. N.B: some of harmful mediator which playing role: - Tumor necrosis factors (TNF). - Interlukine (IL-6). - Platelet activation factor (PAF). - Prostaglandins (Prostacyclin and Thromboxane). - Nitric acid (potent vasodilator) 37 General Surgery 2. Microcirculation: 1. Cytokines vasodilatation  Arterio-Venous shunts. The results are:  Reduced peripheral resistance.  Hypoxia.  Sluggish circulation  DIC 3. vascular endothelial damage - Under the effect of cytokines - Leads to leak of protein rich fluid (third space loss) resulting in oedema. 4. Cellular derangement: (see hypovolemic shock) 5. Acid-Base imbalance, (see hypovolemic shock) 6. Systems and organs, (see hypovolemic shock). Clinical picture: Hyperdynamic (warm) Stage: (SIRS)        Fever above 38°C and chills. Tachycardia and tachypnea. Patient is flushed with warm dry extremities. Restlessness and confusion. Oliguria. Mild reduction in blood pressure. The cardiac output is elevated. Hypo dynamic (cold) Stage: (MOSF)      Reduced cardiac output. Systolic blood pressure < 90 mmHg. Tachycardia and tachypnea. Cold clammy skin. Multiple organ failure starts at this stage (MOSF). Monitoring; See hypovolemic shock. Diagnosis: by: 1. 2. 3. 4. Elevated TLC. Elevated lactate level in blood. Source of sepsis. Blood culture. 38 General Surgery Treatment: (better in ICU) Fighting infection : 1. Immediate recognition and early eradication of the source of sepsis. 2. Antibiotics:  Broad spectrum, till culture and sensitivity.  Commonly combination of cephalosporin, aminoglycosides & metronidazole. Support Systems 1. Cardiovascular support:  Fluid replacement:  Aim to reach CVP (5-10 cm H20) or PAWP (12-15 mm Hg)  Medications:  Inotropic: as dopamine  Vasopressor: Norepinephrine. 2. Respiratory support: - 100% oxygen. - Reduction < 60 mmHg  mechanical ventilation. 3. Renal support: - Adequate volume replacement & dopamine. 4. Control of blood sugar. 5. prophylaxis against DVT and stress ulceration. Monitoring: ( see before) Prognosis:  mortality ranges from 25%- 90%.  Death is usually the result of failure to institute therapy soon enough. 39 General Surgery Neurogenic shock Paralysis of the vasomotor fibers → peripheral vasodilatation → peripheral pooling of blood → inadequate venous return → decrease cardiac output → shock. Causes : /. Vaso-Vagal attack : due to trauma to one of target areas(ear drum, testicles)→excessive vagal stimulation → Bradycardia → Hypotension. 2. High transection of the spinal cord in spine fracture or following spinal anaesthesia → vasomotor sympathetic paralysis → hypotension. Treatment: (1) The patient should lay flat, elevation of the legs help to increase venous return. (2) Crystalloids like Ringer's lactate. (3) Vasopressor drugs may be needed. Cardigenic shock Definition: Inadequate tissue perfusion due to myocardial dysfunction, cardiac index < 2.2 L/Min/m2 + pulmonary artery pressure > 16mmHg and a systolic blood pressure < 90mmIIg. PathophysioIogy: C.O →  systolic pressure → hypotension → tissue hypoperfusion → picture of shock (neck Veins congested and C.V.P. is high). Treatment : 1 . Potent analgesics in myocardial infarction. 2. Oxygen administration. 3. Inotropics → to  cardiac contractility. 4. Vasodilators r→ after load of the heart. 5. Mechanical support by intra-aortic balloon counter - pulsations. Anaphylactic Shock  Antigen exposure  antigen and antibody releases histamine, cytokines and other vaso-active substances that cause: 1. vasodilatation and increased capillary permeability. 2. bronchospasm, laryngeal oedema and respiratory distress.  The common causes in practice are: 1. Penicillin injection 2. I.V. radiological contrast media. Sometimes wasps and bee stings in some people 40 General Surgery Traumatic Shock and Burn Shock - They are 2 descriptive types of shock combining more than one cause  Traumatic shock: Hypovolaemia associated with cardiogenic shock.  Burn shock: If involving more than 20% of the body surface. It is due to loss of plasma from the capillaries. If infection occurs later endotoxaemia is added. Assessment of Shock Skin colour Sweating Temperature Capillary refill CVP Hypovolaemic Pale Cardiogenic Pale Septic Flushed Anaphylactic Urticarial rash Present Cold Present Cold Absent Warm Absent Warm Slow Slow Rapid Low High Low Normal or Rapid Low Resuscitation: 1. ABCDE protocol is followed (In case of trauma). 2. Insert two large canulae (14) in a peripheral vein and start with Ringer lactate. 3. Provision of 100% oxygen via a face mask. 4. Venous blood samples are taken for measuring Hb, Hematocrit, blood glucose, urea, electrolytes and cardiac enzymes. 5. Also blood grouping and cross matching are done if haemorrhage is the cause. 6. If sepsis is suspected a blood sample is taken for aerobic culture and antibiotic sensitivity. 7. A urinary catheter is fixed and urine output is documented hourly. 8. 41 General Surgery Complication of shock SIRS & MODS Pathophysiology: 1- Inititiating factor: - Usually Gram-negative infection. - Endotoxins pass to the circulation  stimulates macrophages  Cytokines that mediate the inflammatory response. - Exotoxins released by staph aureus act directly on T cells  Cytokine release. 2- Macrophage-cytokine release: - Results in the release of TNF- α, IL-1 and IL-6. - There is also inhibition IL-2 production. 3- Microcirculatory injury: - Reperfusion of tissues after ischaemia causes the release of toxic oxygen radicals. - These cause tissue damage causing release of cytokines. 4- Gut barrier failure: - Loss of mucus and increase in permeability. This allows bacterial translocation. - Kupffer's cells in the liver lose their filtering power and allow bacteria and endotoxins to enter the systemic circulation. - Hepatocytes may be damaged leading to jaundice. 5- Mechanism of end-organ faliure: - Continuous release of cytokines and oxygen radicles continue. - Microthrombi are formed, and Interstitial oedema - Organ function deteriorates, and finally damage to the cell membrane. Clinical Picture - Typically: Hypermetabolism 2-3 days following proper resuscitation. At first B.P. is normal, skin is warm and there is increased cardiac output. Later B.P falls, cardiac output remains high  finally decreases. Metabolic acidosis. Diagnosis of SIRS 2 or more of the following are present.  Tachypnea.  Tachycardia  Fever and leucocytosis 42 General Surgery Diagnosis of MODS: 2 or more end organs fail e.g  Respiratory = ARDS - Increased minute ventilation Diminished pulmonary compliance Diminished PaO2 Increased PaCo2  Renal = ARF: - Oliguria  Rising blood urea   Hypoalbuminaemia   Finally anuria  Liver - Jaundice Prolonged PT  Gastro-intestinal - Gastric stress ulcers, Adynamic ileus, Acalculous cholecystitis and Pancreatitis.  Haematology - Leucopenia and DIC  CNS - Confusion and finally coma. Treatment: - The best therapy is prevention: avoid hypotension, gross sepsis, ensure adequate oxygenation and urinary output. There are 4 aims of the treatment 1-Treat infection: 1. Eradicate the source of infection: Drain abscess, remove necrotic tissue ..etc 2. Broad-spectrum Antibiotics. 3. Do blood cultures with antibiotic sensitivity. 4. Prevent nosocomial infection. 43 General Surgery 2-Adequate tissue oxygenation: 5. I.V. fluid therapy with monitoring of CVP, urinary output and PAWP. 6. Inotropic support: Dopamine, Dobutamine, Dopexamine, Adrenaline and Noradrenaline. 7. Diuretics used after hydration is achieved. 8. Ventilatory support with oxygen or mechanical ventilation in severe cases. 3-Nutrition: - Essential to restore the gut barrier function and reduces bacterial translocation. - Enteral feeding is preferred but if not possible TPN is necessary. 4-Minimizing systemic inflammatory response: under trials Use of monoclonal antibodies to TNF- α, IL-1 and IL-6 1. Use of IL-2 to restore T-cell function 2. Use of recombinant protein C (anticoagulant protein) it helps to prevent DIC. Treatment of ARDS 1. Intermittent positive pressure ventilation IPPV 2. If not enough Positive end expiratory pressure ventilation PEEP. 3. Measures to reduce oedema: I.V. albumin and diuretics. Treatment of acute renal failure 1. Fluids limited to 400 ml per day + known losses. 2. Rising K+ is controlled by I.V. glucose and insulin and Ca gluconate. 3. I.V Sod. bicarbonate. 8.3% to control acidosis. 4. If K+ rises above 7 mEq/l haemodialysis or peritoneal dialysis is done. 5. With recovery a diuretic phase  large urine with high loss of Na+ and K+ which will need correction Prognosis of SIRS and MODS  The overall mortality is 7% for SIRS  14% for sepsis syndrome  40% for established septic shock.  Each organ failure has a mortality of 30%.  Patient with 3 or more system failures have mortality rate of 90-95%. 44 General Surgery Metabolic response to injury Definition:  Metabolic disturbances follow all forms of trauma (operations, burns and fractures,…)  Proportionate to the severity of the trauma and to the nutritional state of the patient.  At first (6:8 days): Catabolic.  Followed (10-60 days) by an anabolic phase with repair of tissue, repletion of stores of fat and proteins and weight gain. It is controlled by growth hormone, androgens and ketosteroids. Catabolic Phase: 1. ↓Water excretion: - Increased of ADH from the posterior pituitary. - In the first 24:48 hours urine excretion is reduced to 500 ml per day. 2. ↓Sodium excretion: - Drops from 100 mEq to 10 mEq per day. - Due to Increased secretion of aldosterone. - The duration is 5:6 days. - Independent on whether Na+ is given or not. 3. ↑Potassium: - Increased urinary excretion (maximal the day of operation to 48hours). - It increases from 70:100 mEq to 100:140 mEq. - It is due to mobilization and excretion of intracellular K+. 4. ↑Protein: - Increase the nitrogen excretion from a normal of 10:12 gm daily to 30 gm/day. - Skeletal muscle breakdown  Aminoacids used for gluconeogenesis and proteins. - Through the adrenocortical hormones. (abscent in Addison's disease) 5. ↑Glucose: - Glycogen breakdown  blood glucose level rises - Due to Adrenaline and Glucagon. - Also stimulation of gluconeogenesis from amino-acids due to increased cortisol. - known as diabetis of injury. 6) Fat: - Under control of interleukins and TNF. - Lipases release glycerol and fatty acids. - Glycerol is used for gluconeogenesis and fatty acids are oxidised for energy. 45 General Surgery Anabolic phase - Starts from the second week and may last for several weeks. There is a positive nitrogen balance (3:5 gm nitrogen per day). The patient will gain weight and strength. The responsible factors are the growth hormone and gonadal hormones. later the patient restores body fat previously lost. Objective of Metabolic Response 1. Mobilization of nitrogen and K+  raw materials for the healing of wounds 2. Conservation of Na+ and water  maintain plasma volume after haemorrhage. 3. A well-nourished person shows catabolism vigorously  heals well. While the malnourished dose not  wound dehiscence or non-union of fractures. Practical Applications: 1. First 24:48 hours after operation water is administered excessively, water intoxication results. An overload of 1.5 litres  neausea and disorientation. An overload of 2.5 litres  metal lethargy. If more  convulsions and coma. 2. Excessive administration of saline in the early post-operative period  Na+ retention and secondarily water retention. 3. Administration of K+ in the first 24hours after operation  high level of K in the blood. ----------------------------------------- A system for post-operative fluid administration: 1. In the first 24hours give 2 litres of glucose5%. 2. On the following day give 2litres of glucose 5% and 500ml of saline. 3. From the 4th day add 20mEq of K+ is added to each litre to give a total of 50 mEq/day. 46 General Surgery Blood Transfusion & Blood products Indication for Blood Transfusion: (restore blood volume).  In acute haemorrhage.  During major operation.  Postoperatively after major surgery.  Preoperative blood transfusion is needed if Hb is less than ↓ 8 gm/dl.  To arrest haemorrhage in haemorrhagic states. Blood Sparing Strategies 1. Pre-operative autologous blood donation:  In elective surgery where blood will be lost and where Hb is at least 11-12 gm/dl.  If the blood is not used it will be wasted  If the patient needs more blood the advantage is lost. 2. Erythropoietin:  Used in the anaemia associated with renal failure and in major surgery.  It is given subcutaneously 600 u/kg 3 times weekly and on the day of surgery.  It is usually given with oral or I.V. iron therapy. 3. Acute Normovolemic Haemodilution:  Following induction, 1000 ml of blood are removed and replaced with crystalloids.  The blood is given to the patient when it is needed during or after the surgery.  The patients Hb must be initially high. 4. Intraoperative Blood Salvage:  In clean operations using the cell saver equipment.  Aspirates, anticoagulants and filters the extravasated blood.  Then red cells are washed and given as packed red cells. It is usually used in liver transplantation. 47 General Surgery Blood and blood products I) Stored whole blood:  Collected into a sterile plastic bag.  The bag contains 75 ml of anticoagulant solution CPDA (Citrate Phosphate Dextrose Acid).  Stored at 4°C and can be used within 21 days.ood and blood products  Disadvantage of stored blood 1. Citrate anticoagulant 2. Has an acid pH (6.6-6.8) 3. High level of K+ (from stored red cells) 4. High ammonia (from red cells adenosine) 5. Reduced red cell (2,3-DPG)  impaired release of oxygen from oxy-Hb. 6. White blood cells and platelets are destroyed after 24 hours in the stored blood. 7. Also the levels of clotting factors V and VIII fall quickly. II-Blood fractions 1. Packed Red Cells:  Used in chronic anemia, elderly, cardiac and children and will avoid overload.  The plasma is replaced by 100 ml of a crystalloid solution containing NaCl, adenine, glucose and mannitol (SAG-M blood). 2. Platelet Rich Plasma:  It is prepared by centrifugation of freshly donated blood.  It is used in thrombocytopenia and during surgery. 3. Platelet Concentrate:  Prepared by centrifugation of platelet rich plasma.  They also carry HLA antigens.  reaction (with repeated transfusion).  Indications: Thrombocytopenia, DIC, Massive transfusion, aplastic anaemia. 48 General Surgery 4. Plasma Products: a.Human albumin 4.5%: It is prepared by repeated fractionation of plasma followed by heat treatment. Free from the danger of transmission of hepatitis. Stored for several months in liquid form at 4°C. It is used in burns and in hypoproteinaemia. There is salt-poor human albumin 20% used in cirrhotic patients with ascites. b.Fresh-Frozen Plasma FFP: Plasma removed from fresh blood and rapidly frozen and stored at -40°C. It is a good source of all the coagulation factors, albumin and immunoglobulins. It is used during surgery on liver failure, in Christmas disease and haemophilia. It is not used as plasma expander. c. Cryoprecipitate:  FFP at -4°C, a glutinous precipitate remains.  It is stored at -40°C. Very rich source of factor VIII, Von Willebrand factor and fibrinogen.  Used in treatment of haemophilia, Von Willibrand's disease and is given I.V. d. Factor VIII and factor IX concentrates:  They are now available in freeze-dried form. e. Fibrinogen:  Used in severe depletion of fibrinogen e.g. DIC  Carries a high risk of hepatitis. f. Immunoglubins Ig G:  Provide passive immunity to non-immunised patients exposed to serious infection (viral or bacterial) e.g. human tetanus immunoglogin. 49 General Surgery Changes occur during storage of blood Red cell viability Platelet viability Coagulation factor V & XIII Potassium content (mmol/L) 0 days 95% 95% 95% 3.5 7 days 90% 0% 30% 10 14 days 85% 0% 30% 25 21 days 75% 0% 30% 30 Indications for transfusion Product Whole blood Indication Class III % haemorrhage Precaution Storage life ABO &Rh. 21 days Packed RBC Severe anaemia ABO &Rh. 21 days FFP Bleeding due to non-specified coagulation factor deficiency. coumarin overdose. ABO 1 year at -40 °C Platelet Primary or secondary thrombocytopenia ABO 24-72 hours ABO 1 year at -40 °C Cryoprecipitates Bleeding with fibrinogen depletion VIII & fibrinogen. Factor VIII Factor IX Haemophilia A. Haemophilia B. coumarin overdose. 2 years Albumin Acute volume expansion. Hypoalbuminaeia. 4 years 50 General Surgery Complication of Blood Transfusion I - Transfusion- related complication: 1. Haemolytic reactions. Aetiology:  Antibodies in the recipient's blood against antigens of the donor's cells.  Mostly due to human error. Clinically  Present after the transfusion of less than 50 ml.  Fatal more than 200 cc  Fever, chills, constricting pain in the chest, dyspnoea and pain In the flanks.  tachycardia and hypotension  Anaesthetized patients: haemolytic reactions are sudden tachycardia, hypotension and bleeding tendency.  Major hemolytic reaction will lead to  haemoglobinuria, jaundice and acute renal failure, DIC. Management  Stop transfusion  Send for repeat typing and matching.  Infusion of Lactated Ringer and IV corticosteroids.  Osmotic diuretic as mannitol may be needed.  IV infusion of sodium bicarbonate may be indicated. 2. Pyrogenic reactions.     Commonest complication. Present by: chills, fever, headache, nausea and vomiting. Due to minor bacterial contamination. Transfusion is stopped and the patient is given IV aspirin or paracetamol. 3. Allergic reactions.  