Q7. Write a note on fluid balance in patients and surgery.
Explain the normal water distribution in body.
Ans.
y Total body water—60% of total body weight in males and 50% of total body weight in females (as females have more subcutaneous fat), most water is in skeletal muscles y Of the total body water
– 40% is intracellular
– 15% is interstitial [includes 2% transcellular (water in CSF and joint spaces)]. The interstitial water has a rapidly equilibrating component and slowly equilibrating transcellular component
– 5% intravascular (15% of this is arterial)
y Serum osmolarity = 2 sodium + urea/2.8 + glucose/18 (Normal—280–310 mosm/kg) y The tendency of solute exchange is determined by osmolarity
y The tendency of water exchange is determined by tonicity
y Tonicity is thus relative osmotic activity of two solutions, e.g. azotemia is a hyperosmotic condition but not a hypertonic condition
y Therefore osmolarity of the extracellular fluid is determined primarily by sodium, whereas the effective osmotic pressure between plasma and interstitium is determined by nondiffusible proteins and tonicity = 2 sodium + glucose/18
y Osmolar gap = measured – calculated osmolarity which is due to ethanol, methanol, ethylene glycol and unidentified toxins
y Major intracellular cations include potassium, calcium and major intracellular anions include proteins and phosphates.
y Major extracellular cation include sodium and anions include chloride and bicarbonate.
Contd...
Fluid losses and gain in body
Intake 2000–2600 mL/day
Urine 500–800 mL/day
Insensible loss 600 mL/day (75% from skin, 25% from lungs)
Stool 250 mL/day
Important electrolyte values to remember
In mEq/L Sodium Potassium H+ chloride Bicarbonate Osmolarity
Sweat 50 5 50 50 0
Gastric 50 0 90 100 0
Bile 150 5 0 80 70
Pancreatic 150 5 0 80 110
Colon 120 30 0 80 30
Ileostomy 100 10 0 50 50
Diarrhea 50 50 0 20 40
Ringer lactate 130 4 0 109 Lactate 28, calcium 3 273
Normal saline 154 0 0 154 0 308
Q8. Enumerate the causes of hyponatremia.
Discuss the clinical features and management of a patient with hyponatremia.
Ans. Normal level—135 to 145 mmol/L Causes
Sodium and water loss Euvolemic hyponatremia Water and sodium excess (Water >> sodium) Renal
y Diuretics
y Mineralocorticoid deficiency y Osmotic diuresis (Glucose,
mannitol, urea) y Renal tubular acidoses Extrarenal
y Vomiting y Diarrhea y Burns y Pancreatitis y Rhabdomyolysis
SIADH Hypothyroidism Psychogenic polydipsia Glucocorticoid deficiency
Nephrotic syndrome Congestive cardiac failure Cirrhosis
Acute and chronic renal failure
Clinical features y Headache, confusion
y Weakness, fatigue, muscle cramps
y Anorexia, nausea, vomiting, watery diarrhea, lacrimation, salivation y Hypertension, bradycardia, oliguria
Management
y Hypovolemic hyponatremia: Isotonic saline administration
y Euvolemic hyponatremia: Water restriction
y Hypervolemic hyponatremia: Sodium and water restriction
y Free water excess should be corrected first and then correction of low sodium y If neurological symptoms are present, they should be treated with 3% saline
y Otherwise, treat with 0.9% saline and the rate of treatment should not exceed 12 mEq/L/
day as rapid correction can lead to central pontine myelinolysis now better known as osmotic demyelination syndrome which can have both pontine and/or extrapontine myelinolysis which causes seizures, weakness, akinetic movements and finally permanent brain damage
y Formula for sodium deficit calculation
y Sodium deficit = total body water (130 – measured) Volume—sodium deficit/154 (saline in liters) Q9. Enumerate the causes of hypernatremia.
Discuss the clinical features and management of a patient with hypernatremia.
Ans.
Causes
Sodium and water loss Euvolemic hyponatremia Water and sodium excess (Sodium >> water) Renal
y Loop diuretics
y Osmotic diuresis (Glucose, mannitol, urea)
Extrarenal y Diarrhea y Burns
y Nasogastric aspirations
Diabetes insipidus
Insensible losses from skin and respiratory tract Psychogenic hypodipsia
Primary aldosteronism Cushing syndrome Hypertonic dialysis Bicarbonate infusion
Clinical features
y Restlessness, ataxia, lethargy, irritability, tonic spasm, delirium, coma y Weakness, oliguria
y Dry sticky mucus membrane, red swollen tongue, decreased saliva and tears y Tachycardia and hypotension
Management
y Initially, water deficit should be corrected first then, hypernatremia correction is decided by following formula:
– Water deficit (liters) = total body water (sodium – 140)/140.
y Again, correction should not be done at a rate greater than 12 mEq/L/day.
Potassium balance is very important topic both for exams and for managing patients in clinics and therefore is explained in detail.
Normal potassium homeostasis (Normal—3.5–4.5 mEq/L)
y Total body potassium = 50 mEq/kg body weight. Extracellular is 2% of this and only 0.4% is in plasma. Rest is intracellular.
y Therefore, 1 mEq/L change in potassium in serum is caused by either – An intracellular deficit of around 200–400 mEq or
– Potassium excess of 100–200 mEq
y It is the value which is to be corrected to solve the patient’s problem.
Q10. Enumerate the causes of hypokalemia.
Discuss the clinical features and management of a patient with hypokalemia.
Ans.
Causes
Renal causes Extrarenal causes
y Type I and II renal tubular acidoses y Acetazolamide
y Diabetic ketoacidoses y Uretrosigmoidostomy
y All causes of metabolic alkalosis y Hypomagnesemia
y Bartter syndrome, Gitelman syndrome
y Diarrhoea y GI fistulas y Villous adenoma y Anorexia nervosa y Laxative abuse y Drugs
y Hypokalemic periodic paralysis y Hyperaldosteronism
Spurious hypokalemia: Extreme leucocytosis
Redistributive hypokalemia: Theophylline toxicity, barium toxicity, insulin therapy, etc.
Drugs causing hypokalemia: Aminoglycosides, amphotericin, cisplatin, foscarnet and ifosfamide
Clinical features y Ileus, constipation
y Decreased reflexes, fatigue, weakness, paralysis y Cardiac arrest and/or ECG changes as follows:
Flattened or inverted T waves, a U wave, ST depression and a wide PR interval. The prominent U wave is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval.
y Physiological variation: Potassium decreases by 0.3 mEq/L for every 0.1 increase in pH above normal.
Management
y First step is restoration of volume
y Symptomatic hypokalemia: Give potassium 20 mEq IV over 1 hour under ECG guidance for maximum 4 doses. Rate of correction should not exceed 20 mEq/hour in any case and if at all it is required, it should always be done through a peripheral venous line.
Maximum tolerated limit for potassium correction under ECG guidance is 100 mEq/hr.
y If still not corrected: Look for hypomagnesemia, as untreated hypomagnesemia can lead to resistant hypokalemia which will not be corrected till the magnesium level is corrected.
y Asymptomatic patients: Give oral syrup potassium chloride mixed with water, also add coconut water, bananas and other potassium rich sources.
Q11. Enumerate the causes of hyperkalemia.
Discuss the clinical features and management of a patient with hyperkalemia.
Ans.
Causes
Spurious of hyperkalemia y Tight tourniquet y Hemolysis
y Leucocytosis/thrombocytosis Redistribution of hyperkalemia y Hyperglycemia
y Succinylcholine, digitalis y Hyperkalemic periodic paralysis High renin, low aldosterone y Addison disease
y Heparin and ACE inhibitors Low rennin, low aldosterone y Hyporeninemic hypoaldosteronism
y Cyclosporine toxicity End organ damage with high aldosterone Renal tubular damage due to:
y Autoimmune—SLE, amyloidoses y Hemolysis—sickle cell disease
y Drugs—spironolactone, triamterene and amiloride
Drugs causing hyperkalemia: Angiotensin receptor blockers, ACE inhibitors, digoxin, spironolactone, succinylcholine, heparin, cyclosporin, pentamidine, triamterene.
Clinical features y Colic, diarrhea y Nausea, vomiting
y Weakness, paralysis, respiratory failure y Arrhythmias as follows:
Mild hyperkalemia (5.5–6.5 mEq/L) y Peaked T waves y Prolonged PR segment Moderate hyperkalemia (6.5–8 mEq/L) y Loss of P wave
y Prolonged QRS y ST elevation y Ectopics
Severe hyperkalemia (> 8 mEq/L) y Progressive widening of QRS complex y Sine wave appearance
y Fascicular blocks/bundle branch blocks y Ventricular fibrillations
y Asystole
Management
y First step is restoration of volume.
Therapies
y Calcium: Used only for arrhythmia stabilization. It has no effect on potassium level. It should always be given with cardiac monitoring.
2 solutions : Calcium gluconate 10%=0.5 mL/kg slow IV injection or calcium chloride 10%=0.1–0.2 mL/kg slow IV injection.
y Salbutamol: [K+ sequestrant]. Given by nebulisation or IV y Insulin/Glucose to be given at the same time (K+ sequestrant) y Bicarbonate: In metabolic acidosis only
y Dialysis (K+ excretion) y Kayexalate (K+ excretion) Severe hyperkalemia
Any patient with K+ >7.0 mEq/L or at risk of increasing and/or patient symptomatic and/or ECG disturbance:
Manage with the following measures:
y Calcium IV if ECG changes, salbutamol nebulization, insulin/glucose IV, bicarbonate IV if metabolic acidosis
y Dialysis
y Kayexalate (Polystyrene sulfonate) PR (if dialysis unavailable) Moderate hyperkalemia
Any patient with K 6 to 7 mEq/L, asymptomatic with normal ECG Manage with following measures:
y Salbutamol nebulization, insulin/glucose IV, kayexalate (polystyrene sulfonate) PR or oral, bicarbonate IV if metabolic acidosis
Mild Hyperkalemia
Any patient with K >5.5, asymptomatic with normal ECG Management
y Stop K supplements
y Salbutamol nebulization, bicarbonate IV if metabolic acidosis.
Q12. Enumerate the parameters useful to decide acid-base disorders and give their normal values.
Answer
pH 7.35–7.45
PaO2 74–82 mm Hg
PaCO2 35–45 mm Hg
SaO2 >92%
CaO2 16–20 vol %
HCO3– 22–26 mEq/L
Important buffering systems in body y Intracellular—proteins and phosphates
y Extracellular—bicarbonate-carbonic acid system
Q13. Discuss the steps of diagnoses of an acid-base disorder in a patient.
Explain the mechanism of identification of an acid-base disorder and show its compensation mechanism.
Ans. Acid base imbalances are diagnosed as follows:
1st step: Identify the primary acid-base disorder (Mnemonic—ROME – Respiratoy has Opposite change between pH and pCO2 whereas Metabolic has Equal direction change between ph and bicarbonate)
ABG pH PaCO2 HCO3 Compensation
Metabolic acidoses Decrease N Decrease Decrease in PaCO2
Metabolic alkalosis Increase N Increase Increase in PaCO2
Respiratory acidoses Decrease Increase N Increase in HCO3 Respiratory alkalosis Increase Decrease N Decrease in HCO3
2nd step: Identify compensation as shown in the chart above 3rd step: See if gaps are present in case of metabolic acidoses y Anion gap
Unmeasured cations (UC) (Mn: PCM) Unmeasured anions (UA) (Mn: SOAP) Potassium, calcium and magnesium Sulphate, organic acids, albumin, phosphate
Total – 11 mEq/L Total – 23 mEq/L
Anion gap = UA – UC = 12 mEq/L = sodium – (chloride + bicarbonate) Adjusted anion gap = 2.5 (4.5 – albumin) + observed anion gap.
High anion gap acidoses Normal anion gap acidoses Ethanol/ methanol/propylene glycol poisoning
Salicylates Isoniazid toxicity
Ketoacidoses (Diabetes/starvation/alcohol) Lactic acidoses
Uremia
Proximal (Type 2), distal (Type 1) and Type 4 Renal tubular acidoses
Early renal failure
Exogenous ammonium chloride or HCl Administration
Diarrhea
Carbonic anhydrase inhibitor therapy
y Gap-gap in acidoses: It is calculated only when anion gap is present
Gap-gap = anion gap excess/bicarbonate deficit = (measured anion gap-12)/(24 – measured bicarbonate)
y If gap-gap <1, it indicates co-existence of normal anion gap acidoses with high anion gap acidoses
y If gap-gap >1, it indicates co-existence of metabolic alkalosis with high anion gap acidoses.
Clinical features of acid-base imbalance are as shown in the table on the next page:
Q14. Write a note on metabolic acidoses (above matter + following matter will make the SN).
Ans.
y First step is restoration of volume
y Management mainly aims at correction of the underlying cause
y Sodium bicarbonate is given only when ph < 7.1/sodium bicarbonate < 15 mEq/L y Base deficit = 0.6 body weight (i.e. TBW) (15 – sodium bicarbonate) in mEq/L y Half of this value is administered bolus and half added in the infusion form
y However, sodium bicarbonate has dubious role in management of metabolic acidoses less severe than this and especially in patients with lactic acidoses.
Symptoms of acidoses Symptoms of alkalosis Headache, sleepiness, coma, dyspnea,
arrhythmias, nausea, vomiting, diarrhea, seizures, weakness
Nausea, vomiting, muscle twitches, tremors, numbness, confusion, coma, tingling in hands and feet.
Q15. Explain: Metabolic alkaloses.
Ans.
Causes
Chloride responsive Chloride unresponsive y Respond to chloride administration
y Has low chloride in plasma and urine y Does not respond to chloride administration y Does not have low chloride in plasma and urine y Post-hypercapnea
y Diuretic therapy y Villous adenoma y Gastric aspirations
y Laxative abuse y Bartter syndrome y Primary aldosteronism y Cushing syndrome
y Malignant or accelerated hypertension
Management
y First step in management of any fluid electrolyte or acid-base disorder is the correction of fluid abnormality, i.e. hypovolemia
y Final management depends on correction of cause y Chloride deficit = 0.3 body weight (100 – chloride level) Volume to replace = chloride deficit/154 in liters of isotonic saline y H+ deficit = 0.5 body weight (actual – desired bicarbonate) Volume to replace = H+ deficit/100 in 0.1N HCl.
Q16. Write a note on plasma expanders.
Ans.
Rationale
y Crystalloids redistribute after intravenous administration in a ratio of 1:3 that is for 1 part that remains in the intravascular compartment, 3 parts go into the interstitium.
For example, if 1 liter crystalloid is administered, 750 mL goes into interstitial space and 250 mL remain in intravascular space
y Colloids on the other hand distribute 3:1, that is opposite of crystalloids and thus are called plasma expanders. These are large molecules with poor diffusibility which create an osmotic pressure to increase fluid in intravascular space
y Therefore to counteract blood loss, volume to be transfused y Crystalloid—3:1
y Colloid—1:1
Plasma expanders include y 5% albumin
y 25% albumin (latest) y 6% dextran
y 6% hetastarch
Conflicts
y No convincing evidence that colloids are better than crystalloids.
y No convincing evidence that one colloid is better than other colloid.
Adverse events
y Decreases immunoglobulin response y Decreases albumin production y Decreases ionised calcium level y Decreases response to tetanus toxoid y Increases ECF volume deficit
y Dextran interferes with cross matching and it causes coagulopathy y Hetastarch decreases vWF and factor 8c levels and causes coagulopathy y Hetastarch also causes macroamylesemia.
25% albumin has been found to have some advantages over other colloids in new studies y It has proven anti-inflammatory effect, volume requirement is 5 times less and it has no
coagulopathic side effects
y However, 25% albumin causes only fluid shift in body. Therefore, it should not be used in cases of acute volume loss unless some volume is restored
Hetastarch: It is a starch polymer (6%) in isotonic saline y High molecular weight—4.5 lacs
y Medium molecular weight—2 lacs y Low molecular weight—70,000 daltons
y Hextend—6% hetastarch solution with a buffered multi-electrolyte solution Dextran 70 has a longer duration of action than dextran 40
y None of these fluids have definite preferential advantages over others y All of them have minimal risk of allergic/anaphylactic reactions.