3. Fluid ,Electrolytes and acid base balance
in urology
By
Abdelrahman M Abderkader
Resident of Urology
Assuit University Hospital
2018
4. The French physiologist Cluade
Bernard was the first to discuss
Milieu Interieur,
Hemostais in French,1855.
5. What is an electrolyte ??
• Substance when dissolved in solution separates into ions & is able to carry an
electrical current.
• Important terminology:
Osmalarity-> It is fluid’s capability to create osmotic pressure.
* Osmolality refers to the total concentration of solutes in water.
Effective osmolality is the osmotic gradient created by solutes that do
not cross the cell membrane. Effective osmolality determines the
osmotic pressure and the flow of water.
6. •The body is mainly made of water ,
45%-75% of total body weight is water
according to sex and age .
•The total body water is divided according to
their site into intracellular and extracellular
compartments .
•2/3 intracellular 70%
•1/3 extracellular 30%.
9. ELECTROLYTE BALANCE
A. Physiology of electrolytes
Electrolytes are particles or solutes found throughout the body in fluids.They carry
an electrical charge and are essential for fluid and acid base balance within the
body
The four major functions of electrolytes are:
1. Regulate Acid Base Balance
2. Maintain Fluid Balance and Osmolarity
3. Distribute the Body Fluid and H20 Between the Compartments
4. Promote Neuromuscular Function/Irritability
B. Distribution of electrolytes
Electrolytes are found in the intracellular and extracellular fluid. They are
concentrated in one of these two compartments and exert osmotic properties
within that compartment.Electrolytes help to maintain total body fluid balance and
also help to regulate fluid movement in and out of the cell.For example K+is the
major intracellular ion and Na+is the major extracellular ion and they each play a
significant role in maintaining homeostasis within each of their compartments.
Each electrolyte serves a unique physiologic function and concentrations.
10.
11. THE MOST IMPORTANT SIX ELECTROYTES
•-sodium,
•-potassium
•-chloride
•-bicarbonate
•-calcium
•-phosphate.
12. SODIUM
Na
Sodium is the major cation of the extracellular fluid. It is
responsible for one-half of the osmotic pressure gradient that
exists between the interior of cells and their surrounding
environment. Sodium is an essential mineral that regulates blood
volume, blood pressure, osmotic equilibrium and pH
humans require only 1 to 2 mmol/day or 0.5gm. Excretion of
sodium is accomplished primarily by the kidneys. Sodium is freely
filtered through the glomerular capillaries of the kidneys, and
although much of the filtered sodium is reabsorbed in the
proximal convoluted tubule, some remains in the filtrate and
urine, and is normally excreted.
13. In order to understand the pathophysiology or the effects of sodium excess or decrease on the
human body the Physician must know the basic hormonal and renal regulators of Na excretion
(Renal and Extra-renal mechanism).
RENAL
*99% OF the filtered sodium is reabsorbed: 65% in proximal tubule, 25% in the loop of Henle & 10%
in the distal convoluted tubule.
a-The glomerular filtration rate.
b-Renin-Angiotensin mechanism VIA juxtaglomerular apparatus.
C-prostaglandins.
-the angiotensin 2 stimulate sodium reabsorption from all segments &constrict the glomerular
capillary Which lead to sodium retention and restore of ECF volume.
EXTRARENAL
1-antidiuretic hormone (adh)
2- Renin-Angiotensin mechanism Via Aldersterone
3-antinatriuretic peptide (anp).
14. ADH
• Produced in supraoptic nucleus in the hypothalamus then released to
posterior pituitary In response to increased osmolality by osmoreceptors in
the hypothalamus <INCREASED Na CONC INRELATION TO ECF>
• the ADH is released in response to
- Reduced blood pressure
- Reduced Blood volume
- Angiotensin 2
Also ADH lead to
1-increase permeability of dct to water
2-vasoconstriction
3- it stimulate drinking
16. RENIN ANGIOTENSIN ALDESTERONE SYSTEM
• RENIN is produced in response
-Reduced to arterial blood pressure.
-Reduced sodium in the plasma sensed by macula densa.
-Increased sympathetic activity.
The production RENIN lead to production of ANGIOTENSIN 2.
• ANGIOTENSIN 2 lead to
-Vasoconstriction of arteries
-Increased drinking
-Production of ALDOSTERONE
-Production of ADH
17. ALDOSTERONE
• Aldosterone tends to promote Na+ and water retention, and lower plasma K+ concentration
by the following mechanisms
1-Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal
tubule and the collecting duct of the kidney nephron, it upregulates and activates the
basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial
fluid and two potassium ions into the cell from the interstitial fluid. This creates a
concentration gradient which results in reabsorption of sodium (Na+) ions and water (which
follows sodium) into the blood, and secreting potassium (K+) ions into the urine (lumen of
collecting duct).
2-Aldosterone upregulates epithelial sodium channels (ENaCs) in the collecting duct and the
colon, increasing apical membrane permeability for Na+ and thus absorption.
3-Cl− is reabsorbed in conjunction with sodium cations to maintain the system's electrochemical
balance.
4-Aldosterone stimulates the secretion of K+ into the tubular lumen.
5-Aldosterone stimulates Na+ and water reabsorption from the gut, salivary and sweat glands
in exchange for K+.
6-Aldosterone stimulates secretion of H+ via the H+/ATPase in the intercalated cells of the
cortical collecting tubules.
18.
19. • Normal Na level in plasma is 135-150 &
normal Na level in urine is 75-200)/24h.
• The sodium below 110 is considered to be critical (alarming) must
take action to correct.
• The sodium above 160 is considered to be critical (alarming) must
take action to correct.
20. The Hyponatremia is two types:
Depletional & Dilutional
DEPLETIONAL HYPONATREMIA:
1-Renal losses 2-non renal losses
a-Diuretics a-GIT vomiting and diarrhea
b-HYPOALDOSTERONISM b-skin burns
c-ADDISONS DISEASE
d-D.M
E-POLYURIC PHASE OF ACUTE RENAL FAILURE
F-SALT LOSING NEPHEROPATHY
DILUTIONAL HYPONATREMIA
1-SIADH (syndrome of inappropriate secretion of antidiuretic hormone)
2-congestive heart failure
3-liver cirrhosis
4-renal failure
21. Another classification
• Excess of extracellular water relative to sodium content of
extracellular compartment
it occur in three different circumstances
a-Hypovolemia
b-Hypervolemia
c-Normovolemia
(Neurosurgical patient as in brain tumors or trauma,
polydipsia, lymphoma, meningitis, lung abscess and stress)
22. Hypovolemic Hyponatremia
There are numerous causes of hypovolemic hypernatremia. Patients typically have signs and symptoms
associated with volume depletion (e.g., vomiting, diarrhea, tachycardia, elevated blood urea nitrogen–
to-creatinine ratio). Urinary sodium levels are typically less than 20 mEq per L unless the kidney is the
site of sodium loss.
Fractional excretion of sodium is often inaccurately elevated in patients receiving diuretics because of
diuretic-induced natriuretic; fractional excretion of urea can be utilized in these patients instead.
Fractional excretion of urea less than 35% is more sensitive and specific for diagnosing prerenal
azotemia in this setting.
Treatment generally consists of volume repletion with isotonic (0.9%) saline, occasional use of salt
tablets, and treatment of the underlying condition. Monitoring of urine output is recommended
because output of more than 100 mL per hour can be a warning sign of overcorrection.
23. Euvolemic hyponatremia
• Euvolemic hyponatremia is most commonly caused by SIADH, but can also be caused by hypothyroidism
and glucocorticoid deficiency. Euvolemia is diagnosed by findings from the history and physical
examination, low serum uric acid levels, a normal blood urea nitrogen–to-creatinine ratio, and spot urinary
sodium greater than 20 mEq per L. Diuretic therapy can artificially elevate urinary sodium, whereas a low-
salt diet can artificially lower urinary sodium, thus clouding the diagnosis of hypovolemia vs. euvolemia.
• Treatment generally consists of fluid restriction and correcting the underlying cause. Fluid restriction
should be limited to 500 mL less than the daily urinary volume. Salt and protein intake should not be
restricted.
• Predictors of failure with fluid restriction include urinary osmolality greater than 500 mOsm per kg, 24-
hour urinary volume less than 1.5 L, an increase in the serum sodium level of less than 2 mEq per L within
24 to 48 hours, and a serum sodium level less than the sum of the urinary sodium and potassium levels.
Volume status can be difficult to determine; therefore, a trial of intravenous fluids may be
warranted.Sodium levels in patients with SIADH will decrease further with intravenous fluid
administration. The use of demeclocycline (Declomycin) and lithium is not recommended because of an
increased risk of harm.
24. Hypervolemic Hyponatremia
Hypervolemic hyponatremia occurs when the kidneys cannot excrete water
efficiently. In volume overload states, the effective arterial blood volume is
decreased compared with venous volume, resulting in excess ADH secretion.
The most common causes of hypervolemic hyponatremia are heart failure,
cirrhosis, and kidney injury. Treatment consists of correcting the underlying
cause, sodium and fluid restriction, and diuretic therapy to increase excretion of
solute-free water.13,14 A randomized controlled trial of 46 patients with heart
failure showed that restricting fluid intake to 1 L per day improved quality of
life 60 days after discharge.
28. • Treatment of hyponatremia
1-Restrict fluids
2-Monitor VitalSigns
3-Monitor serum Na levels
4-IV normal saline or Lactated Ringers
5-If Na is below 115, mEq/L hypertonic saline is ordered
6-May give a diuretic for increasing H2O loss
29. • Severe symptomatic hyponatremia must be corrected promptly because it
can lead to cerebral edema, irreversible neurologic damage, respiratory
arrest, brainstem herniation, and death.
• Treatment includes the use of hypertonic 3% saline infused at a rate of
0.5 to 2 mL per kg per hour until symptoms resolve. At this time, vaptans
have no role in the treatment of symptomatic hyponatremia because of
the potential for overcorrection of sodium and variable sodium
fluctuations.(Vaptans conivaptan [Vaprisol] and tolvaptan [Samsca]) are
vasopressin-receptor antagonists approved for the treatment of
hospitalized patients with severe hypervolemic and euvolemic
hyponatremia Loop diuretics may be needed in patients with concurrent
symptomatic hyponatremia and volume overload. The rate of sodium
correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq per
L or less in 48 hours.12–14 An increase of 4 to 6 mEq per L is usually
sufficient to reduce symptoms of acute hyponatremia. Rapid correction of
sodium can result in osmotic demyelination (previously called central
pontine myelinolysis). Overcorrection is common and is typically caused
by rapid diuresis secondary to decreasing ADH levels.
30.
31.
32. Potassium
• Potasium is a major intercellular cation.only 2% of body
potassium is in ECF. The normal range in serum 3.5-5.5mmol/L.
• Panic serum level if less than 2.5mmol/L and more than
6.5mmol/L.
36. Treatment
• Treatment including addressing the cause, such as improving the diet, treating diarrhea, or
stopping an offending medication. People without a significant source of potassium loss and who
show no symptoms of hypokalemia may not require treatment.
Mild hypokalemia (>3.0 meq/l) may be treated with oral potassium chloride supplements (Klor-
Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing
foods may be recommended, such as leafy green vegetables, avocados, tomatoes, coconut water,
citrus fruits, oranges, or bananas.[20] Both dietary and pharmaceutical supplements are used for
people taking diuretic medications.
Severe hypokalemia (<3.0 meq/l) may require intravenous supplementation. Typically, a saline
solution is used, with 20–40 meq/l KCl per liter over 3–4 hours. Giving IV potassium at faster rates
(20–25 meq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A
generally safe rate is 10 meq/hr. Even in severe hypokalemia, oral supplementation is preferred
given its safety profile. Sustained-release formulations should be avoided in acute settings.
Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic,
such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia
will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake .
38. treatment
• Insulin (e.g. intravenous injection of 10-15 units of regular insulin along with 50 ml of 50%
dextrose to prevent the blood sugar from dropping too low) leads to a shift of potassium ions into
cells, secondary to increased activity of the sodium-potassium ATPase.[33] Its effects last a few
hours, so it sometimes must be repeated while other measures are taken to suppress potassium
levels more permanently. The insulin is usually given with an appropriate amount of glucose to
prevent hypoglycemia following the insulin administration.
• Salbutamol (albuterol), a β2-selective catecholamine, is administered by nebulizer (e.g. 10–20
mg). This medication also lowers blood levels of K+ by promoting its movement into cells.[33]
• Sodium bicarbonate may be used with the above measures if it is believed the person has
metabolic acidosis
• Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of
removing potassium from the body
• Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlorthalidone,
hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with
intact kidney function.
Fludrocortisone, a synthetic mineralocorticoid, can also increase potassium excretion by the
kidney in patients with functioning kidneys. Trials of fludrocortisone in patients on dialysis have
shown it to be ineffective
39. Tur Syndrome.
• Trans Urethral Resection of Prostate (TURP) is the second most common surgical procedure (after cataract
extraction) done in men over the age of 65 years.
• Though it is called TURP Syndrome, this complication can occur during other endoscopic
procedures also namely Uretero-Renoscopy (URS), Percutaneous Nephrolithotomy (PCNL),
Trans Cervical Resection of Endometrium (TCRE), etc. Despite improvements in the current
surgical and anesthetic management, 2.5 - 20% of patients undergoing TURP show one or
more manifestations of TURP syndrome and 0.5% - 5% die perioperatively.
• True TURP syndrome is now rare, particularly as glycine-based irrigation fluids are less commonly used.
• ***PATHOPHYSIOLOGY-****:
--SIMPLY IT IS fluid overload and Iso-osmolar Hyponatraemia.
Mechanism of clinical manifestations
* symptoms primarily arise from the effects of glycine, which acts as an inhibitory CNS
neurotransmitter at GABA receptors and paradoxically potentiates NMDA receptors
*Increased plasma ammonia may also contribute
* glycine also has cardiodepressant effects and may have renal toxicity
-(not (usually) from increased brain water!)
40. Factors affecting amount and rate
of fluid absorption:
*Size of gland (25ml/gm of prostate)
*Number and size of open sinuses
*Hydrostatic pressure of irrigating fluid
*Duration of procedure (@ 20-30 ml/min)
*Integrity of capsule
*Venous pressure at irrigant-blood interface
*Vascularity of diseased prostate
41. IRRIGATION FLUID CHARCTERS:
• transparent (for good visibility)
• electrically non-conductive (to prevent dispersion of the
diathermy current)
• isotonic
• non-toxic
• non-haemolytic when absorbed
• easy to sterilize
• inexpensive
42. • CLINICAL FEATURES
• Timing
it may occur within 15 minutes or be delayed for up to 24 hours post-operatively
typically lasts hours.
• Early features
mild cases may go unrecognized,- restlessness, headache, and tachypnoea, or a
burning sensation in the face and hands
*Features of greater severity
• respiratory distress, hypoxia, pulmonary oedema
• nausea, vomiting
• visual disturbance (e.g. blindness, fixed pupils)
• confusion, convulsions, and coma
• haemolysis
• acute renal failure
43. *Features of greater severity
• respiratory distress, hypoxia, pulmonary oedema
• nausea, vomiting
• visual disturbance (e.g. blindness, fixed pupils)
• confusion, convulsions, and coma
• haemolysis
• acute renal failure
• reflex bradycardia from fluid absorption
Symptoms may be masked by general anaesthesia and severe cases
may present with dysrhythmias and cardiovascular collapse
44. • Laboratory
• hyponatraemia (dilutional effect of a large volume of absorbed irrigation
fluid, but later due to natriuresis)
• iso-osmolar (or mildly hypo-osmolar)
• increased osmolar gap from absorbed glycine
• hyperglycinaemia (up to 20 mM; normal is 0.15-0.3mmol/L)
• hyperserinaemia (major metabolite of glycine)
• hyperammonaemia (due to deamination of glycine and serine)
• hyperoxalataemia and hypocalcaemia (glycine is metabolised to
glycoxylic acid and oxalic acid, the latter forms calclium oxalate crystals in
the urinary tracts and may contribute to renal failure)
• metabolic acidosis
• haemodilution and haemolysis
45. • MANAGEMENT
• Resuscitation
• Attend to ABCs and address life threats:
• O2 +/- intubation (or airway protection) and ventilation
• invasive monitoring
• Specific Treatment
1 fluid overload: frusemide 40mg IV
2 seizures: benzodiazepines +/- other anti-epileptics; consider magnesium (stabilises NMDA
receptors)
3 hyponatreamia:
- hypertonic saline is only indicated for neurological manifestations if measured serum
osmolality is < 260 mOsmol/kg
- aim to raise Na+ by no more than 10-12 mmol/24 hours)
- a rapid increase in plasma sodium is not concerning (this often happens with glycine
metabolism), unless there is a sudden change in osmolality (measured osmolality usually changes
little as the hyponatremia resolves)
• severe cases may require renal replacement therapy
• treat acute pulmonary oedema and dysrhythmias as required
• treat hypocalcaemia
