fluid and electrolyes

1. FLUID AND ELECTROLYES IN
SURGICAL PATIENTS
MODERATOR:
PROF.DR.SHASHIKALA .CK
PRESENTED BY:
MRIDUL.GS

2. COMPOSITION OF BODY FLUIDS
• Water is the most abundant constituent in the body, accounting for
50% of body weight in women, 60% in men and 75-80% in neonates
• Total body water is distributed in two major compartments: 2/3rd is
intracellular [intracellular fluid (ICF)], and1/3rd is extracellular
[extracellular fluid (ECF)].
• ECF is further subdivided into intravascular (plasma water) and
extravascular (interstitial) spaces in a ratio of 1:3.

3. TOTAL BODY WATER

4. Fluid and electrolytes
• Fluid intake is derived from both exogenous (consumed liquids) and
endogenous (released during oxidation of solid foodstuffs) sources
Average daily water balance of a healthy adult in a temperate climate
(70 kg)
Output Volume(ml) Intake Volume (ml)
Urine 1500 Water from beverage 2000
Insensible losses 900 Water from food 200
Feces 100 Water from oxidation 300

5. `
• Fluid losses occur by four routes:
1. Lungs. About 400 ml of water is lost in expired air per day. This is
increased in dry atmospheres or in patients with a tracheostomy,
emphasising the importance of humidification of inspired air.
2. Skin. In a temperate climate, sweat losses are between 600 and
1000 ml/d which increases in a tropical country like India
3. Faeces. Between 60 and 150 ml of water are lost daily in patients
with normal bowel function.
4. Urine. The normal urine output is approximately 1500 ml/d. A
minimum urine output of 400 ml/d is required to excrete the end
products of protein metabolism.

6. Type of fluids
Colloids
Colloids are a group of fluids containing large molecules designed to
remain in the intravenous space longer than crystalloid fluids. Colloids
are commonly termed plasma expanders. Colloids are used in cases of
shock where cardiovascular function needs to be improved rapidly:
• Haemorrhage
• Shock
• Severe dehydration.

7. 1.Gelatins
• Gelatins are straw coloured, isotonic colloid solutions. The two trade
names in common use are Haemaccel™ and Gelofusin™.
• Gelatins should be stored at room temperature. They are administered
through a standard fluid administration set and intravenous catheter.
• The patient does not require cross-matching before administration and
gelatins must not be administered with whole blood.
2.Plasma
Plasma is also considered in the colloid category. Whole blood can be
separated, e.g. by centrifugation, into plasma and packed red cells. It allows
the patient to receive specific treatment with plasma proteins, while
minimising the risk of a cross-reaction as compared to whole blood

8. 3.Albumin preparations
• Albumin preparations ultimately distribute throughout the
extracellular space, although the initial location of distribution is
the vascular compartment.
• Albumin is indicated in the edematous patient to mobilize
interstitial fluid into the intravascular space.
• They are not indicated in the patient with adequate colloid
oncotic pressure (serum albumin >2.5 mg/dL, total protein >5
mg/dL), or as a nutritional source.

9. 4. Dextran
• Dextran is a synthetic glucose polymer that undergoes predominantly
renal elimination.
• Dextran solutions expand the intravascular volume by an amount
equal to the volume infused.
• Side effects include renal failure, osmotic diuresis, coagulopathy, and
laboratory abnormalities (i.e., elevations in blood glucose and protein
and interference with blood cross-matching).
• Preparations of 40- and 70-kD dextran are available

10. Crystalloids
Crystalloids are a group of sodium-based electrolyte fluids.
1. Hartmann’s (lactated Ringer’s) solution
• Hartmann’s contains electrolytes in very similar concentrations to
those in the extracellular fluid (ECF). Sodium, potassium, calcium,
chloride and lactate are present.
• Hartmann’s is indicated in many cases of fluid and electrolyte losses.
The lactate present is metabolised to bicarbonate, and this is used in
the body to overcome situations of metabolic acidosis, which occur in
many clinical conditions.
2. 0.9% sodium chloride (Normal saline)
• This solution contains sodium and chloride , but no potassium.
• indicated in fluid and electrolyte losses, particularly when plasma
potassium levels are increased due to underlying disease

11. 3. 5% dextrose
• 5% dextrose, also referred to as 5% glucose, is basically water with a
small amount (50 mg/mL) of glucose added in order to make it
isotonic.
• This solution contains no electrolytes so provides the body with water
and a very small amount of glucose.
• 5% dextrose is indicated in situations of primary water loss, where the
patient is unable to take in oral fluids, and in cases of hypoglycaemia.
The amount of glucose present is too little to make a significant
contribution to the energy intake
4. Dextrose saline
• Dextrose-saline is mainly water but also has a small amount of
sodium and chloride to replace daily urinary losses in the normal
person.
• It is used in cases of primary water loss and as a maintenance fluid

12. 5. Ringer’s solution
• Ringer’s solution contains mainly sodium, chloride and some
potassium.
• Indicated in water and electrolyte loss when there is also some
potassium deficit.
• It is mainly used in cases of pyometra when severe vomiting is
present.
6. Darrow’s solution
• This solution contains sodium, chloride, and potassium in higher
concentrations than Ringer’s or Hartmann’s.
• Darrow’s solution is mainly indicated in cases of metabolic acidosis
with potassium deficiency, e.g. persistent diarrhoea.

13. Composition of crystalloid and colloid solutions (mM/L)
SOLUTION SODIUM POTASSIUM CALCIUM CHLORIDE LACTATE COLLOID
Hartmann’s (Ringer’s lactate)
Ringer’s solution
Normal saline (0.9% NaCl)
Dextrose saline (5% dextrose in
0.9% saline)
Gelofusine
Haemacel
Hetastarch
Isolyte G
Isolyte M
130
147
154
154
150
145
65
40
4
4
5.1
17
35
2.7
2.5
<1
6.26
109
156
154
154
150
145
150
38
28
29
Gelatin 4%
Polygelin 75g/L
Hydroxyethyl starch 6%
NH4
+
59
PO4
3-
15, Acetate 20

14. Fluid and electrolye is an important
aspect for the care of surgical
patients…Why?

15. • Acute stress>Increase sympathetic stimuli>tachycardia
,vasocontriction and stress
• ACTH secretioin increases>increase hydrocorticosterone
>aldosterone>sodium retention and potaasium loss
• Major surgery >hypovolemia>aldostreone> so 1st 2-3 postop days
leads to decresed sodium requirment

16. • Postop Pain and stress >increase ADH>in 1st 2-3 postop days >water
retention>decrease urine output..in 1st post op period so
maintenance fluid in 1st op period is lesser.
• NPO before ot>replace pre or intraop
• Patient who is hypovolemia prior to surgery is very likely to become
hypotensive during surgery hence correct it preop.

17. • Fluid therapy in surgical patients
1) Pre op
2) Intra op
3) Post op

18. Preop
Correction of hypovolemia
Correction of anaemia
Correction of other disorder

19. Correction of hypovolemia in preop why
necessary?
• Hypovolemia>affects O2 transport>hypoxia >organ failure
• Moreever uncorrected hypovolemia is compensated by increased
vascular ressitence and heart rate due to normal baroreceptor
reflexes preop>but on induction>these reflex intreputed>severe
hypotension and even ARF.

20. How to evaluate?
• Mild(<2liter)
Thirst ,concerated urine
Moderate (2-3 liter)
Diziness,weakness,oliguria(<400 ml/day),low jvp,postural hypo
Severe(>3 litre)
Confusion,stupor,sytolic<100,tachy,low volume pulse,cold extremities

21. Causes-Surgical pateints
• Vomiting,nasogastric
suction,fever,hyperventi,diuretic,diarrhoea,preop bowel prep.
3rd space loss(dedestribution of ECF)-Massive ascites,crush injury,acute
intestinal obstruction,acute gastric dilatation,acute peritonitis,acute
pancreatitis,acute severe cellulitis,

22. How to correct?
• ECF defecit (L)= 0.2 *lean body weight *(Current Hct/Normalhct -1)
• Roughly
Mild- 4 percent bodyweight
Moderate 6-8%
Severe-10 %
Eg:50 kg> 5 liter>normal saline choice…>Ringer lactate and colloids and
whole bloood can be used.
In severe >intially 1000ml per hour

23. • Effective rate of fluid repalcement per hour= 50-100 ml +urine output
per hour+Ongoing loss

24. How to monitor
• Improvement in tachy,BP,acheving urine output > 30-50 ml per hour.

25. Preop correction of anemia why?
• Proper tissue oxygenation intraop and post op….
WHEN to give?
48-72 hour prior to surgery
Why?
Stored blood less 2,3 DPG ..restoration takes 48 hour..

26. Correction of other factors
• Fluid overload_mainly in CHF ,renal faliure,cirrhosis
• Hypokalemia-Mainly GI losses(vomiiting,nasogastric
aspiration,ureteroentrostomies),parentral
nutrition,diuretics,metabolicalkolosis
Patient with hypokalemia are at risk of developing cardiac arrhytmias
intraop and resp difficulty after extubation and parlytic ileus post op.

27. • Hyperkalemia-Severe injury,acidosis,pottasium rich fluid in oliguric
/anuric renal failure.

28. Intraop fluid therapy Why?
• Loss of blood,fluid depeltion,third space loss,evaporative loss from
visera,hypoxia,vasodilatory effect of anesthetic agents and spinal or
epidural anesthesia.
RL is most widely used.

29. correction
• Volume to be replaced for starvtion fluid deficit:Duration of
starvation(Hour)*2ml/kg
• Maintenance volume of intraop= duration of sx*2ml/kg
• Usual fluid loos intraop
• Type of sx- Least trauma-nil, minimal-4ml/kg
• Moderate- 6ml/kg ,severe-10 ml/kg

30. • Eg: Appendectomy>npo 10 hour,1 hour surg, moderate trauma..
• 10*2*50=1000ml, 1*2*50=100ml,6*50=300ml ,total=1400ml

31. Post op fluid therapy
Goal is to maintain:BP>100,Pulse <120, hourly urine output 30-50 ml .
Usual prescription of postop IV fluid
First 24 hour- 2litre 5%D or 1.5L 5%D +500ml saline
2nd postop-2litre 5%D +1 litre saline
3rd day-Similar fluid + 40-60 meq pottasium per day

32. When IV fluid containing saline is prefered?
• Elderly patient with salt losing nephropathy
• Head injury
• Patient on diuretics
• To replace nasogastric aspiration
• In most of major surgery,saline is given to replace third space losses.

33. Postop fluid electrolye problems:
• Volume excess:
Excessive infusion,turp.
Hyponatemia: Stress >ADH>retention of water
Turp
SIDAH in neurosugical patients
Post op with exculsively with 5%D
Hypernatermia:excessive saline,post head injury,diabetes
insipidus,excessiv ewater loss in hypergylecmia

34. • Hypokalemia:GIT loss:Diarrhoea ,nasogastric loss, metabolic
alkalosis
• Post op diuretic
• Hyperkalemia:Crush injury, severe injury,surgical stress, renal
failure.

36. Serum electroytes in surgical patients

37. Sodium
• Principle cation in the ECF
• Major ion responsible for determining the tonicity of plasma
• N: 135-145mEq/L
• Disorders of serum Na+ concentration are caused by abnormalities in
water homeostasis that lead to changes in the relative ratio of Na+ to
body water.
• Water intake and circulating AVP constitute the two key effectors in
the defense of serum osmolality; defects in one or both of these
defense mechanisms cause most cases of hyponatremia and
hypernatremia

38. Hyponatremia
• Defined as a plasma Na+ concentration <135 mM, is a very common
disorder, occurring in up to 22% of hospitalized patients.
• This disorder is almost always the result of an increase in circulating
AVP and/or increased renal sensitivity to AVP, combined with any
intake of free water
• Hyponatremia is subdivided diagnostically into three groups,
depending on clinical history and serum osmolality: hypotonic,
isotonic, and hypertonic.

40. Isotonic hyponatremia.
• Hyperlipidemic and hyperproteinemic states result in an isotonic
expansion of the circulating plasma volume and cause a decrease in
serum Na+ concentration, although total body Na+ remains
unchanged.
• The reduction in serum sodium (mmol/L) can be estimated by
multiplying the measured plasma triglyceride concentration (mg/dL)
by 0.002 or the increase in serum protein concentration above 8 g/dL
by 0.25.
• Isotonic, sodium-free solutions of glucose, mannitol, and glycine are
restricted initially to the extracellular fluid and may similarly result in
transient hyponatremia.

41. Hypertonic hyponatremia
• Hyperglycemia may result in a transient fluid shift from the
intracellular to the extracellular compartment, thereby diluting serum
Na+ concentration.
• The expected decrease in serum Na+ is approximately 1.6 mmol/L for
each 100-mg/dL increase in blood glucose above 200 mg/dL.

42. Hypotonic hyponatremia
Hypotonic hyponatremia is classified on the basis of extracellular fluid
volume into
1. Hypovolemic
2. Hypervolemic
3. Euvolemic
Hypotonic hyponatremia generally develops as a consequence of the
administration and retention of hypotonic fluids [e.g., dextrose 5% in
water (D5W) and 0.45% NaCl] and rarely from the loss of salt-
containing fluids alone.

43. Hypovolemic hypotonic hyponatremia
Hypovolemic hypotonic hyponatremia in the surgical patient most
commonly results from replacement of sodium-rich fluid losses (e.g.,
from the GI tract, skin, or lungs) with an insufficient volume of
hypotonic fluid (e.g., D5 W and 0.45% NaCl).

44. Hypervolemic hypotonic hyponatremia
• The edematous states of congestive heart failure, liver disease, and
nephrosis occur in conjunction with inadequate circulating blood
volume.
• This serves as a stimulus for the renal retention of sodium and of
water.
• Disproportionate accumulation of water results in hyponatremia.

45. Isovolemic hypotonic hyponatremia
i. Water intoxication typically occurs in the patient who consumes
large quantities of water and has mildly impaired renal function
(primary polydipsia). Alternatively, it may be the result of the
administration of large quantities of hypotonic fluid in the patient
with generalized renal failure.
ii. K+ loss, either from GI fluid loss or secondary to diuretics, may
result in isovolemic hyponatremia due to cellular exchange of
these cations.

46. iii. Reset osmostat. Seen in chronic diseases (e.g., tuberculosis and
cirrhosis). These patients respond normally to water loads with suppression
of antidiuretic hormone (ADH) secretion and excretion of free water.
iv. SIADH is characterized by low plasma osmolality (<280 mOsm/L),
hyponatremia (<135 mmol/L), low urine output with concentrated urine
(>100 mOsm/kg), elevated urine sodium (>20 mEq/L), and clinical euvolemia.
The major causes of SIADH include
•pulmonary disorders (e.g., atelectasis, empyema, pneumothorax, and
respiratory failure),
•central nervous system disorders (e.g., trauma, meningitis, tumors, and
subarachnoid hemorrhage),
•drugs (e.g., cyclophosphamide, cisplatin, and nonsteroidal anti-
inflammatory drugs),
•ectopic ADH production (e.g., small-cell lung carcinoma).

47. Transurethral resection syndrome
Transurethral resection syndrome refers to hyponatremia in
conjunction with cardiovascular and neurologic manifestations, which
infrequently follow transurethral resection of the prostate.
This syndrome results from intraoperative absorption of significant
amounts of irrigation fluid (e.g., glycine, sorbitol, or mannitol).
Isotonic, hypotonic, or hypertonic hyponatremia may occur.

48. Clinical manifestations:
• Symptoms associated with hyponatremia are predominantly neurologic
and result from hypoosmolality.
• A decrease in Posm causes intracellular water influx, increased intracellular
volume, and cerebral edema.
• Symptoms include lethargy, confusion, nausea, vomiting, seizures, and
coma.
• The likelihood that symptoms will occur is related to the degree of
hyponatremia and to the rapidity with which it develops.
• Chronic hyponatremia is often asymptomatic until the serum Na+
concentration falls below 110 mEq/L.
• An acute drop in the serum Na+ concentration to 120 mEq/L may produce
symptoms

49. Treatment
1. Isotonic and hypertonic hyponatremia correct with resolution of
the underlying disorder.
2. Hypovolemic hyponatremia can be managed with administration of
0.9% NaCl to correct volume deficits and replace ongoing losses.
3. Water intoxication responds to fluid restriction (1,000 mL/day).
4. For SIADH, water restriction (1,000 mL/day) should be attempted
initially. The addition of a loop diuretic (furosemide) or an osmotic
diuretic (mannitol) may be necessary in refractory cases.

50. 5. Hypervolemic hyponatremia may respond to water restriction
(1,000 mL/day) to return Na+ to greater than 130 mmol/L (299 mg/dL).
1. In cases of severe congestive heart failure, optimizing cardiac
performance will assist in Na+ correction.
2. If the edematous hyponatremic patient becomes symptomatic,
plasma Na+ can be increased to a safe level by the use of a loop
diuretic (furosemide, 20 to 200 mg intravenously every 6 hours)
while replacing urinary Na+ losses with 3% NaCl. Approximately
25% of the hourly urine output should be replaced with 3% NaCl.
Hypertonic saline should not be administered to these patients
without concomitant diuretic therapy.
3. Administration of synthetic brain natriuretic peptide (BNP) is also
useful therapeutically in the setting of acute heart failure

51. Treatment of symptomatic hyponatremia
• In the presence of symptoms or extreme hyponatremia [Na+ <110
mmol/L], hypertonic saline (3% NaCl) is indicated. Serum Na+ should
be corrected to approximately 120 mmol/L.
• The rate of correction is calculated as follows
The approximate change in serum sodium concentration by infusing
1 litre of 3% NaCl is calculated using
[Na]= {[Nai] + [Ki] -[Nas]} / {TBW+1}
Where [Nai] and [Ki] are the sodium and potassium concentrations in
the infused fluid and [Nas] is the starting serum sodium
Dividing the desired rate of correction by [Na] gives the
appropriate rate of administration in litres per hour

52. e.g.:An 80 kg woman is seizing. Her Na is 108mEq/L
• Rate of correction: she has symptomatic hyponatremia requiring an acute
correction of 1 mEq/h for first 4 hrs but not more than 12mEq/L over 24 hrs
using hypertonic saline i.e., 0.5mEq/h after 4 hrs
• Means of correction
[Na]={513-108}/{80 X 0.5 + 1} = 10mEq/L
So, 1 litre of hypertonic saline will increase her serum sodium by 10mEq/L
So the rate of fluid to be infused in first 4hrs is
Rate=desired rate/ [Na]
=[1mEq/L/hr] / [10mEq/L per 1L of solution
=100mL/hr

53. Hypernatremia
• Defined as a plasma concentration of >145mmol/dL
• Hypernatremia is usually the result of a combined water and
electrolyte deficit, with losses of H2O in excess of those of Na+

54. HYPERNATREMIA

55. Hypovolemic hypernatremia
• Any net loss of hypotonic body fluid results in extracellular volume
depletion and hypernatremia.
• Common causes in the surgical patient include diuresis as well as GI,
respiratory, and cutaneous (e.g.,burns) fluid losses.
• Chronic renal failure and partial urinary tract obstruction also may
cause hypovolemic hypernatremia.

56. Hypervolemic hypernatremia
Hypervolemic hypernatremia in the surgical patient is most commonly
iatrogenic and results from the parenteral administration of hypertonic
solutions (e.g., NaHCO3, saline, medications, and nutrition).

57. Isovolemic hypernatremia
a. Hypotonic losses.
• Constant evaporative losses from the skin and respiratory tract, in
addition to ongoing urinary free water losses, require the
administration of approximately 750 mL of electrolyte-free water
(e.g., D5 W) daily to parenterally maintained afebrile patients.
• Inappropriate replacement of these hypotonic losses with isotonic
fluids is the most common cause of isovolemic hypernatremia in the
hospitalized surgical patient.

58. b. Diabetes insipidus is characterized by polyuria and polydipsia in
association with hypotonic urine (urine osmolality <200 mOsm/kg or a
specific gravity of <1.005) and a high plasma osmolality (>287
mOsm/kg).
Central diabetes insipidus (CDI) describes a defect in the hypothalamic
secretion of ADH and is commonly seen after head trauma or hypophysectomy.
and also as a result of intracranial tumors, infections, vascular disorders
(aneurysms), hypoxia, or medications (e.g., clonidine and phencyclidine).
Nephrogenic diabetes insipidus (NDI) describes renal insensitivity to normally
secreted ADH. NDI may be familial or drug induced (e.g., lithium,
demeclocycline, methoxyflurane, and glyburide) or intrinsic renal disease.
.

59. c.Therapeutic. Hypertonic saline may be administered for deliberate
hypernatremia to control elevated intracranial pressure (ICP) and
cerebral edema after head injury

60. Clinical manifestations.
• Symptoms of hypernatremia that are related to the hyperosmolar
state are primarily neurologic.
• These initially include lethargy, weakness, and irritability
• Later progress to fasciculations, seizures, coma, and irreversible
neurologic damage.

61. Treatment
1. Water deficit associated with hypernatremia can be estimated using
thefollowing equation .
Water deficit(L)=0.6(body weight) [serum Na/140-1]
• Rapid correction of hypernatremia can result in cerebral edema and
permanent neurologic damage. Consequently, only one half of the water
deficit should be corrected over the first 24 hours, with the remainder
being corrected over the following 2 to 3 days.
• Serial Na+ measurements are necessary to ensure that the rate of
correction is adequate
• Oral fluid intake is acceptable for replacing water deficits.
• If oral intake is not possible, D5 W or D5 0.45% NaCl can be substituted.
• In addition to the actual water deficit, insensible losses and urinary output
must be replaced.

62. 2. Diabetes insipidus
a. Central diabetes insipidus :desmopressin acetate administered
intranasally [10 to 40 μg daily] or subcutaneously or intravenously
[2 to 4 μg daily].
b. Nephrogenic diabetes insipidus:
• removal of any potentially offending drug and correction of
electrolyte abnormalities.
• If these measures are ineffective, dietary sodium restriction in
conjunction with a thiazide diuretic may be useful
(hydrochlorothiazide, 50 to 100 mg/day orally).

63. Potassium
• Principal cation in the ICF
• Normal:3.5mEq-5mEq
• In a healthy individual at steady state, the entire daily
intake of potassium is excreted, approximately 90% in the
urine and 10% in the stool; the kidney thus plays a
dominant role in potassium homeostasis
• Kidneys play the major role in potassium homeostasis

64. Hypokalemia
• Hypokalemia, defined as a plasma K+ concentration <3.6 mM, occurs in
up to 20% of hospitalized patients.
• Hypokalemia is associated with a tenfold increase in in-hospital mortality
rates due to adverse effects on cardiac rhythm, blood pressure, and
cardiovascular morbidity rate.
• Mechanistically, hypokalemia is caused by
1. redistribution of K+ between tissues and the ECF
2. renal and nonrenal loss of K+ .
• Spurious hypokalemia or pseudohypokalemia occasionally can result
from in vitro cellular uptake of K+ after venipuncture, for example, due to
profound leukocytosis in acute leukemia.

65. Causes
I. Decreased intake as in starvation- rare
II. Redistribution into cells
A. Acid-base
1. Metabolic alkalosis
B. Hormonal
1. Insulin
2. Increased beta2-adrenergic sympathetic activity: post-myocardial infarction, head
injury
3. beta2-Adrenergic agonists: bronchodilators, tocolytics
4. Thyrotoxic periodic paralysis
5. Downstream stimulation of Na
+
/K
+
-ATPase: theophylline, caffeine

66. Causes contd…
C. Anabolic state
1. Vitamin B12 or folic acid administration (red blood cell production)
2. Granulocyte-macrophage colony-stimulating factor (white blood cell production)
D. Other
1. Pseudohypokalemia
2. Hypothermia
3. Familial hypokalemic periodic paralysis
4. Barium toxicity: systemic inhibition of "leak" K
+
channels
III. Increased loss
A. Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)

67. B. Renal
1. Increased distal flow and distal Na
+
delivery: diuretics, osmotic
diuresis, salt-wasting nephropathies
2. Increased secretion of potassium as in mineralocorticoid excess
3. Magnesium deficiency: Magnesium depletion has inhibitory
effects on muscle Na+,K+-ATPase activity, reducing influx into muscle
cells and causing a secondary kaliuresis.

68. Clinical manifestations
• Hypokalemia has prominent effects on cardiac, skeletal, and
intestinal muscle cells. In particular, it is a major risk factor for
both ventricular and atrial arrhythmias.
• Electrocardiographic changes in hypokalemia include broad flat T
waves, ST depression, and QT prolongation; these are most
marked when serum K+ is <2.7 mmol/L.
• Hypokalemia also results in hyperpolarization of skeletal muscle
leading to weakness and even paralysis. It also causes a skeletal
myopathy and predisposes to rhabdomyolysis. The paralytic
effects of hypokalemia on intestinal smooth muscle may cause
intestinal ileus.
• Hypokalemia can cause a renal resistance to aVP and thus cause
polyuria

69. Treatment.
• Mild hypokalemia:
1. Oral replacement .
2. Typical daily therapy in a patient with intact renal function is 40 to 100 mmol
(156 to 390 mg) KCl orally in single or divided doses.
• Severe hypokalemia
1. Parenteral therapy
2. K+ concentrations (administered as chloride, acetate, or phosphate) in
peripherally administered intravenous fluids should not exceed 40 mmol/L, and
the rate of administration should not exceed 20mmol/hour.
3. Higher K+ concentrations [60 to 80 mmol/L ] administered more rapidly (with
cardiac monitoring) are indicated in cases of very severe hypokalemia, for cardiac
arrhythmias, and in the management of diabetic ketoacidosis.
• Administration of high K+ concentrations via subclavian, jugular, or right atrial
catheters should be avoided because local K+ concentrations may be cardiotoxic.
• Hypomagnesemia frequently accompanies hypokalemia and must be corrected to
replenish K+ effectively.

70. Hyperkalemia
Causes
• Hyperkalemia may occur with normal or elevated stores of total body K+.
• Pseudohyperkalemia is a laboratory abnormality that reflects K+ release from leukocytes and
platelets during coagulation.
• Spurious elevation in K+ may result from hemolysis or phlebotomy from a strangulated arm.
• Abnormal redistribution of K+ from the intracellular to the extracellular compartment is seen
in
1. insulin deficiency
2. β-adrenergic receptor blockade
3. acute acidosis
4. rhabdomyolysis,
5. cell lysis (after chemotherapy)
6. digitalis intoxication
7. reperfusion of ischemic limbs
8. succinylcholine administration

71. Clinical manifestations.
• Mild hyperkalemia [5 to 6 mmol/L]: Asymptomatic.
• Significant hyperkalemia [6.5 mmol/L]:
ECG abnormalities: symmetric peaking of T waves, reduced P-wave
voltage, and widening of the QRS complex. If untreated cases sinusoidal
ECG pattern.

72. Treatment
• Mild hyperkalemia [5 to 6 mmol/L]
1. Conservative treatment
2. Reduction in daily K+ intake
3. If not responding, the addition of a loop diuretic (e.g., furosemide) to
promote renal elimination.
4. Any medication that is capable of impairing K+ homeostasis should
be discontinued, if possible

73. • Severe hyperkalemia [K+ >6.5 mmol/L (25.4 mg/dL)]
a. Temporizing measures produce shifts of potassium from the extracellular to
the intracellular space.
1. NaHCO3 [1 mmol/kg or 1 to 2 ampules (50 mL each) of 8.4% NaHCO 3]
infused intravenously over a 3- to 5-minute period.
This dose can be repeated after 10 to 15 minutes if ECG abnormalities
persist.
2. Dextrose (0.5 g/kg body weight) infused with insulin (0.3 unit of regular
insulin/g of dextrose) transiently lowers serum K+ (the usual dose is 25 g
dextrose, with 6 to 10 units of regular insulin given simultaneously as a
bolus).
3. Inhaled β-agonists [e.g., albuterol sulfate, 2 to 4 mL of 0.5% solution (10 to
20 mg) delivered via nebulizer] have been shown to lower plasma K+, with
a duration of action of up to 2 hours
Caution is warranted in patients with known or suspected cardiovascular
disease.
4. Calcium gluconate 10% (5 to 10 mL intravenously over 2 minutes) should
be administered to patients with profound ECG changes
Calcium functions to stabilize the myocardium.

74. b. Therapeutic measures to definitively decrease total body potassium by
increasing potassium excretion:
1. Sodium polystyrene sulfonate (Kayexalate)
-Na-K exchange resin
-orally (20 to 50 g of the resin in 100 to 200 mL of 20% sorbitol every
4 hours) or
-rectally (as a retention enema, 50 g of the resin in 50 mL of 70%
sorbitol added to 100 to 200 mL of water every 1 to 2 hours initially,
followed by administration every 6 hours) to promote K+ elimination.
-A decrease in serum K + level typically occurs 2 to 4 hours after
administration.
2. Hydration with 0.9% NaCl in combination with a loop diuretic (e.g.,
furosemide, 20 to 100 mg intravenously) should be administered to
patients with adequate renal function to promote renal K+ excretion.
3. Dialysis is definitive therapy in severe, refractory, or life-threatening
hyperkalemia.

75. Calcium
• Normal:8.9-10.3 mg/dL Ionized:4.5-5.3mg/dL
• 12,000 times more in ECF compared to ICF
• Three forms:
1. ionized (45%)- physiologically active
2. protein bound (40%)
3. complex with freely diffusible compounds (15%)
• Normal calcium metabolism is under the influence of parathyroid
hormone (PTH) and vitamin D.
• PTH promotes calcium resorption from bone and reclamation of calcium
from the glomerular filtrate.
• Vitamin D increases calcium absorption from the intestinal tract.

76. Hypocalcemia
• Causes
1. Most commonly occurs as a consequence of calcium sequestration or
vitamin D deficiency.
2. Calcium sequestration may occur in the setting of acute pancreatitis,
rhabdomyolysis, or rapid administration of blood (citrate acting as a
calcium chelator).
3. Transient hypocalcemia may occur after total thyroidectomy,
secondary to vascular compromise of the parathyroid glands, and after
parathyroidectomy.
After parathyroidectomy, serum Ca2+ reaches its lowest level within 2
to 3 days after operation, returning to normal in 2 to 3 days

77. • Hypocalcemia may occur in conjunction with Mg2+ depletion, which
simultaneously impairs PTH secretion and function.
• Acute alkalosis (e.g., from rapid administration of parenteral bicarbonate
or hyperventilation) may produce clinical hypocalcemia with a normal
serum calcium concentration due to an abrupt decrease in the ionized
fraction.
• Because 40% of serum calcium is bound to albumin, hypoalbuminemia
may decrease total serum calcium significantly—a fall in serum albumin
of 1 g/dL decreases serum calcium by approximately 0.8 mg/dL.
• As a consequence, the diagnosis of hypocalcemia should be based on
ionized, not total serum calcium

78. • Clinical manifestations.
1. Tetany is the major clinical finding and may be demonstrated by
Chvostek's sign (facial muscle spasm elicited by tapping over the
branches of the facial nerve).
2. Perioral numbness and tingling.
3. Carpopedal spasm
4. Trosseau sign
5. Qt interval prolongation and ventricular arrhythmias.
6. Seizures, laryngospasm in severe cases

79. Treatment
Oral therapy:
1. Calcium salts are available for oral administration (calcium carbonate,
calcium gluconate).
• Each 1,250-mg tablet of calcium carbonate provides 500 mg of elemental
calcium and a 1,000-mg tablet of calcium gluconate has 90 mg of
elemental calcium.
• In chronic hypocalcemia, with serum calcium levels of 7.6 mg/dL or
higher, the daily administration of 1,000 to 2,000 mg of elemental
calcium alone will suffice.
• When hypocalcemia is more severe, calcium salts should be
supplemented with a vitamin D preparation.
• Daily therapy is initiated with 50,000 IU of calciferol OR 0.4 mg of
dihydrotachysterol OR 0.25 to 0.50 μg of 1,25-dihydroxyvitamin D3
orally. Subsequent therapy should be adjusted as necessary.

80. • Parenteral therapy.
• Indications: Symptoms such as overt tetany, laryngeal spasm, or seizures
• Approximately 200 mg of elemental calcium is needed to abort an attack of tetany.
• Initial therapy consists in the administration of a calcium bolus (10 to 20 mL of 10%
calcium gluconate over 10 minutes) followed by a maintenance infusion of 1 to 2
mg/kg elemental calcium/hour.
• The serum calcium level typically normalizes in 6 to 12 hours with this regimen, at
which time the maintenance rate can be decreased to 0.3 to 0.5 mg/kg/hour
• Calcium chloride contains three times more elemental calcium than calcium gluconate
and can be used as a substitute
1. One 10-mL ampule of 10% calcium chloride = 272 mg elemental Ca
2. One 10-mL ampule of 10% calcium gluconate = 90 mg elemental Ca
• Calcium should be administered cautiously to patients who are receiving digitalis
preparations because digitalis toxicity may be potentiated

81. Hypercalcemia
Causes
• Malignancy
• Hyperparathyroidism
• Hyperthyroidism
• Vitamin D intoxication
• Immobilization
• Long-term total parenteral nutrition
• Thiazide diuretics
• Granulomatous disease

82. • Clinical manifestations
• Mild hypercalcemia (calcium >12 mg/dL): asymptomatic.
• The hypercalcemia of hyperparathyroidism is associated infrequently
with classic parathyroid bone disease and nephrolithiasis.
• Manifestations of severe hypercalcemia include
1. Altered mental status
2. Diffuse weakness
3. Adynamic ileus
4. Nausea and vomiting
5. Severe constipation.
• The cardiac effects of hypercalcemia include QT-interval shortening and
arrhythmias.

83. Treatment
• Mild hypercalcemia (<12 mg/dL):
1. managed conservatively by restricting calcium intake and treating
the underlying disorder.
2. Volume depletion should be corrected if present
3. Vitamin D, calcium supplements, and thiazide diuretics should be
discontinued.

84. SEVERE HYPERCALCEMIA
1. NaCl 0.9% at a rate of 250-500ml/hr and loop diuretics (furosemide
20 mg intravenously every 4 to 6 hours) for 2-3hrs
a) Rate is subsequently adjusted to maintain a urine output of 200 to
300 mL/hour.
b) Mg2+, phosphorus, and K+ levels should be monitored and
repleted as necessary.
c) This treatment may promote the loss of as much as 2 g of calcium
over 24 hours.

85. 2.Salmon calcitonin, in conjunction with adequate hydration, is used in cases
due to malignancy and primary hyperparathyroidism.
a) Salmon calcitonin can be administered either subcutaneously or
intramuscularly.
b) Skin testing by subcutaneous injection of 1 IU is recommended before
progressing to the initial dose of 4 IU/kg intravenously or
subcutaneously every 12 hours.
c) A hypocalcemic effect may be seen as early as 6 to 10 hours after
administration.
d) The dose may be doubled if unsuccessful after 48 hours of treatment.
e) The maximum recommended dose is 8 IU/kg every 6 hours.

86. 3.Pamidronate disodium is used in the treatment of hypercalcemia
associated with malignancy.
• For moderate hypercalcemia (calcium 12 to 13.5 mg/dL), 60 mg of
pamidronate diluted in 1 L 0.9% NaCl should be infused over 24 hours.
• For severe hypercalcemia, the dose of pamidronate is 90 mg.
• If hypercalcemia recurs, a repeat dose of pamidronate can be given after
7 days.
4.Plicamycin (25 μg/kg, diluted in 1 L of 0.9% NaCl ifused over 6 hours
each day for 3 to 4 days) is also used in hypercalcemia associated with
malignancy.
• Onset of action is between 1 and 2 days
• Duration of action is 1 week.

87. PHOSPHOROUS
• Normal: 2.5 to 4.5 mg/dL (0.81 to 1.45 mmol/L).
• Phosphorus balance is regulated by a number of hormones that also
control calcium metabolism.
• As a consequence, derangements in concentrations of phosphorus and
calcium frequently coexist

88. Hypophosphatemia
Causes
• Decreased intestinal phosphate absorption results from vitamin D deficiency,
malabsorption, and the use of phosphate binders (e.g., aluminum, magnesium,
calcium, or iron-containing compounds).
• Renal phosphate loss may occur with acidosis, alkalosis, diuretic therapy (particularly
acetazolamide), during recovery from acute tubular necrosis, and during
hyperglycemia as a result of osmotic diuresis.
• Phosphorus redistribution from the extracellular to the intracellular compartment
1. respiratory alkalosis
2. administration of nutrients such as glucose (particularly in the malnourished
patient).
3. initiation of total parenteral nutrition (refeeding syndrome) as a result of the
incorporation of phosphorus into rapidly dividing cells.
• Hypophosphatemia may develop in burn patients as a result of excessive
phosphaturia during fluid mobilization and incorporation of phosphorus into new
tissues during wound healing.

89. Clinical manifestations.
• Moderate hypophosphatemia (phosphorus 1 to 2.5mg/dL is usually
asymptomatic.
• Severehypophosphatemia (phosphorus <1 mg/dL)
1. respiratory muscle dysfunction
2. diffuse weakness
3. flaccid paralysis.

90. Treatment
• Phosphorus replacement should begin with intravenous therapy, especially for
moderate (1 to 1.7 mg/dL) or severe (<1 mg/dL) hypophosphatemia
• Risks of intravenous therapy include
1. Hyperphosphatemia, hypocalcemia, hyperkalemia (with potassium
phosphate) and hypomagnesemia,
2. Hypotension
3. Hyperosmolality,
4. metastatic calcification, and renal failure.
• 5 to 7 days of intravenous repletion may be required before intracellular stores
are replenished.
• Once the serum phosphorus level exceeds 2 mg/dL (0.65 mmol/L), oral
therapy can be initiated with a sodium-potassium phosphate salt [e.g.,Neutra-
Phos, 250 to 500 mg (8 to 16 mmol phosphorus)

91. HYPERPHOSPHATEMIA
Causes
• impaired renal excretion
• transcellular shifts of phosphorus from the intracellular to the
extracellular compartment (e.g., tissue trauma, tumor lysis, insulin
deficiency, or acidosis).
• Postoperative hypoparathyroidism.

92. Clinical manifestations
• Acute cases: hypocalcemia and tetany.
• Chronic cases: soft tissue calcification and secondary
hyperparathyroidism

93. Treatment
• Aims
1. eliminate the phosphorus source,
2. remove phosphorus from the circulation, and
3. correct coexisting hypocalcemia.
• Dietary phosphorus restriction
• Urinary phosphorus excretion can be increased by hydration (0.9% NaCl at 250 to
500 mL/hour) and diuresis (acetazolamide, 500 mg every 6 hours orally or
intravenously).
• Phosphate binders (aluminum hydroxide, 30 to 120 mL orally every 6 hours)
minimize intestinal phosphate absorption and can induce a negative balance of
greater than 250 mg of phosphorus daily, even in the absence of dietary
phosphorus.
• Hyperphosphatemia secondary to conditions that cause phosphorus
redistribution resolves with treatment of the underlying condition
• Dialysis in very severe cases

94. MAGNESIUM
• Normal:1.5 to 2.3 mg/dL
• Predominantly intracellular
• Renal excretion and retention play the major physiologic role in
regulating body stores.
• Magnesium is not under any direct hormonal regulation

95. Hypomagnesemia
Causes
• Dietary insufficiency is rare
• Excessive GI loss as in diarrhea, malabsorption, vomiting, or biliary fistulas.
• Excessive renal loss as in marked diuresis, primary hyperaldosteronism, renal
tubular dysfunction (e.g.,renal tubular acidosis), or as a drug side effect (e.g.,
loop diuretics, aminoglycosides, and cisplatin).
• Shifts of Mg2+ from the extracellular to the intracellular space seen in acute
myocardial infarction, alcohol withdrawal, or after receiving glucose-
containing solutions.
• After parathyroidectomy for hyperparathyroidism, the redeposition of calcium
and Mg2+ in bone may cause dramatic hypocalcemia and hypomagnesemia.
• Hypomagnesemia is usually accompanied by hypokalemia and
hypophosphatemia and is frequently encountered in the trauma patient

96. Clinical manifestations
• Symptoms are predominantly neuromuscular and cardiovascular.
• With severe depletion, altered mental status, tremors, hyperreflexia, and
tetany may be present.
• The cardiovascular effects are similar to those of hypokalemia and
include T-wave and QRS-complex broadening as well as prolongation of
the PR and QT intervals.
• Ventricular arrhythmias most commonly occur in patients who receive
digitalis preparations.

97. Treatment
• Parenteral therapy is preferred for the treatment of severe
hypomagnesemia (Mg2+ <1 mEq/L or 0.5 mmol/L) or in symptomatic
patients.
• In cases of lifethreatening arrhythmias, 1 to 2 g (8 to 16 mEq) of MgSO4
can be administered over 5 minutes, followed by a continuous infusion
of 1 to 2 g/hour for the next several hours. The infusion subsequently
can be reduced to 0.5 to 1 g/hour for maintenance.
• In less urgent situations, MgSO4 infusion is started at 1 to 2 g/hour for 3
to 6 hours, with the rate subsequently adjusted to 0.5 to 1 g/hour for
maintenance.

98. • Mild hypomagnesemia (1.1 to 1.4 mEq/L or 0.5 to 0.7 mmol/L) in an
asymptomatic patient can be treated initially with the parenteral
administration of 50 to 100 mEq (6 to 12 g) of MgSO4 daily until body
stores are replenished. Treatment should be continued for 3 to 5
days, at which time the patient can be switched to an oral
maintenance dose.
• Intravenous MgSO4 remains the initial therapy of choice for torsades
de pointes (polymorphologic ventricular tachycardia).
• Parenteral Mg is also used to achieve hypermagnesemia that is
therapeutic for eclampsia and pre-eclampsia

99. • Oral therapy
• Magnesium oxide is the preferred oral agent. Each 400-mg tablet
provides 241 mg (20 mEq) of Mg2+.
• Other formulations include magnesium gluconate [each 500-mg tablet
provides 27 mg (2.3 mEq) of Mg2+] and magnesium chloride [each 535-
mg tablet provides 64 mg (5.5 mEq) of Mg2+].
• Depending on the level of depletion, oral therapy should provide 20 to
80 mEq of Mg/day in divided doses.
• Prevention of hypomagnesemia in the hospitalized patient who is
receiving prolonged parenteral nutritional therapy can be accomplished
by providing 0.35 to 0.45 mEq/kg of Mg2+/day [i.e., by adding 8 to 16
mEq (1 to 2 g) of MgSO4 to each liter of intravenous fluids].

100. Hypermagnesemia
Causes
• Hypermagnesemia occurs infrequently, is usually iatrogenic, and is
• seen most commonly in the setting of renal failure.
Clinical manifestations
• Mild hypermagnesemia (Mg2+ 5 to 6 mEq/L or 2.5 to 3mmol/L) is
generally asymptomatic.
• Severe hypermagnesemia (Mg2+ >8 mEq/L or 4 mmol/L) is associated
with
1. depression of deep tendon reflexes,
2. paralysis of voluntary muscles,
3. hypotension,
4. sinus bradycardia, and prolongation of PR, QRS, and QT intervals.

101. Treatment
• Cessation of exogenous Mg2+
• Calcium gluconate 10% (10 to 20 mL over 5 to 10 minutes intravenously)
is indicated in the presence of life-threatening symptoms (e.g.,
hyporeflexia, respiratory depression, or cardiac conduction disturbances)
to antagonize the effects of Mg2+
• A 0.9% NaCl (250 to 500 mL/hour) infusion with loop diuretic
(furosemide, 20 mg intravenously every 4 to 6 hours) in the patient with
intact renal function promotes renal elimination.
• Dialysis is the definitive therapy in the presence of intractable
symptomatic hypermagnesemia.

102. THANK YOU