Electrolyte and acid Base balance

Electrolyte disturbances

Na level
Hypo-natremia and hyper-natremia are water distribution or water balance problem.

Hyponatermia
It's defined as Na concentration <135mEq/L.

To maintain Na concentration, we need to replace of water loss with equal amount of

water excretion. So, problem in elimination of water or expands the water around fixed
Na concentration --> hyponatremia
Osmolarity = 2X Na + glucose/18 and urea/2.8

Note: in renal salt loss, serum osmolarity = urine osmolarity

Urinary osmolarity is important. Normally, in case of hypo-osmolarity, normal response

is to dilute urine (urine osmolarity <100). If not --> ADH release either from appropriate
or not
We measure Na to differentiate between renal and extra-renal loss of Na. If urinary
Na>20 --> urinary source . However, if <10 --> non-urinary loss (meaning poor renal
perfusion)

Expansion of space surrounding Na can occur in many variety

1. Pseudo-hyponatremia: It's a lab phenomenon occurs in hyperlipidemia or increase

plasma protein. These increase non-aqeous portion of plasma--> errant low of Na
concentration. Serum osmolarity is normal !!
2. Hyper-osmolar hyponatremia: in which there is increase in serum osmolarity due
to increase osmotically active solute other than Na --> drawing water into extra-
cellular fluid --> decrease Na level. Most common cause is hyperglycemia. [Na]
decrease 1.6-2.4 mEq/L for every 100mg/dl rise in blood glucose level Other
solutes like glycine, mannitol or sorbitol. These can be absorbed from bladder into
ECF after bladder irrigation causing post-transurethral resection of prostate
(TRUP)
3. Rarely due to water intoxication, excessive water drinking and beer potomania
(tea and toast diet). This is due to fact that there is limit of renal water excretion
accompanied with excessive water drinking or eating solute poor diet. Uine can
not be diluted to become less than 50mOsm/L. So, we need to get rid of some
solutes.

Decrease of water clearance via variety of processes. This is mainly controlled via
vasopressin (anti-diuretic hormone-ADH). Secretion of ADH can be either appropriate or
inappropriate.

1. Appropriate ADH, ADH is released in case of falling of circulating volume and

it's associated with thirst center stimulation. It's subdivided into
a. Hypo-volemic hyponatremia: This is secondary to dehydration (vomiting,
diarrhea, use of diuretic and ACE inhibitors and mineralcorticosteroid
deficiency)
b. Hyper-volemic hyponatremia: nephrotic, cirrhosis and CHF. We have a
decrease circulating blood volume despite increase total body water
2. Inappropriate ADH release: there is ADH secretion in absence of volume
contraction or osmotic stimuli. These patients are typically euvolemic (due to
renal secretion of water). Most important cause is syndrome of inappropriate
ADH (SIADH). Non-physiologic release of ADH. Causes are
a. Neuropsychatric causes: meningitis, encephalitis, acute psychosis head
trauma and cerebrovascular accident.
b. Respiratory like pneumonia, TB and acute respiratory failure
c. Malignancy mainly small cell lung carcinoma
d. Drug induce mainly NSAID, SSRI, cholorpropamide and anti-psychotic
Criteria for SIADH (euvolemic hyponatremia)

 Low serum osmolarity <270

 Urine osmolarity > serum osmolarity
 Urinary Na >20mEq/L
 No hypovolemia (normal BUN:Creatinine ratio)
 No stress inducing ADH release (like post surgery) or other causes of ADH
release
 With giving IV saline, Urinary Na excretion increase with stabilizing serum
Na.
 Rule out hypothyrodism and adrenal failure since it can cause clinical
scenario similar to ADH

3. Reset osmostat: body sets new point for plasma osmolarity and ADH and thirst
response to maintain osmolarity to that level. Classic example is pregnancy

We need to assess circulating volume and ECF status to allow knowing the cause of
hyponatremia
Clinical presentation
 Hyponatremia --> shifting water into intraceullar compartment --> cerebral
edema. So, symptoms develop both on amount of Na fall + rate. In acute decrease
of Na (within 2 days) -->
o at 125 =nausea and malaise
o lower than 125 --> headache, lethargy and confusion
o Stupor, seizure, Coma and death if Na below 115
  In chronic setting (develop >3 days), body minimize increase in ICF --> not much
symptoms

Treatment
We need to determine rate of correction+ appropriate intervention+ treating of co-
existing disease if present

In case of acute hyponatremia, give hypertonic saline. However, we fear from central
pontine myelinolysis (CPM). It's a neurologic damage of neuron secondary to osmotic
shifts. It's characterized via flaccid paralysis, dysphagia and dysarthia. It's diagnosed via
CT or MRI. To avoid CPM, we do not increase [Na] more than 12mEq/L/day.

Now, in acute sever hyponatremia (<115mEq/L) --> increase Na in rate of 1-2 mEq/L/
hour for 3-4 hours then correction rate must tapper off. So, maximum correction is
within 10-12/day.

1 liter of hypertonic saline = 513mEq/L.

We need to memorize the formula

Delta Na=([Nai] + [Ki] -[Nas] ) / (weight X0.6 in male or .5 in female +1)

For example, a 80 Kg female with serum Na is 108mEq/L. If we give 1 liter of

hypertonic saline

513-108/80*.5+1=10. So, giving 1 liter of hypertonic saline --> increase Na via 10

we need 2mEq/L increase per hour. So, 2/10=0.2mEq/L--> give 200ml per hour

Sine we need to avoid CPM, do not give more than 1 liter of hypertonic saline per day.

Asymptomatic hyponatremia

1. Hypovolemia, give isotonic saline to restore circulating volume --> normalization

of Na.
2. Hypervolemia, giving saline will worsen edema. So, we treat the cause (CHF,
nephrotic and cirrhosis). To attenuate hyponatremia,
a. Decrease oral fluid intake
b. Use of loop diuretics --> enhance urination
3. SIADH treatment
a. Mild and asymptomatic hyponatremia (120-130) --> First line is water
restriction between 800-1000 ml/day
b. If asymptomatic with Na 110-120 --> loop diuretic + normal saline
c. If sever (there is seizure or Na <120 + symptoms)--> facilitate urination
via Hypertonic saline (3%) + /- loop diuretic. Other method of treatment
i. Increase salt and protein intake. If no protein, give urea 30-60gram
ii. Vasopressing analogue either IV conivaptan or oral tolvaptan
activating V2 receptor
iii. Lithum and demeclocyline can be used in treating SIADH.
However, they are associated with major side effect and no more
used
Hypernatremia
It's defined as [Na]>145mEq/L and always represents a state of hyper-osmolarity -->
stimulate thirsty center and excretion of maximally concentrated urine.

Causes
 Water deficit, most common cause
o Impaired thirst response, occur in case of limited access to water or most
commonly in due to physical restriction (severely debilitated patient)
o Increase water loss,
 Non-renal loss: diarrhea is most common GI cause of
hypernatremia (viral gastroenteritis and osmotic diarrhea-sorbitol
or carbohydrates malabsorption --> loss water >Na). Others like
loss of water from skin and respiratory tract
 Renal water loss
 Osmotic dieuresis : glycosuria, high protein feed, increase
urea production from accelerated catabolism of protein and
steroid
 DI
o Central (decrease ADH secretion): Most common
cause is destruction of neurohypophysis secondary
to trauma, surgery, infection, vascular accident and
granulomatous disease. Many cases are idiopathic
o Nephrogenic (periphery- resistance to ADH). It can
be secondary to drugs -lithium, demeclocycline and
amphotericin, electrolyte disturbances-hypokalemia
and hypercalcemia, intrinsic renal disease and loop
diuretic
o Gain Na, either from administration of hypertonic saline or chronic
mineral-corticoid excess.

Clinical presentation
  Shifting of water from ICF--> ECF --> shrinking of neurons -->weakness, altered
mental status and neuromuscular irritability. Occasionally, it can cause seizure
and coma
 Chronic hyponatremia less symptoms
 Polyuria and polydipsia in case of CDI/NDI.

Diagnosis
In hypernatremia, urine volume should be low with urine osmolarity >800. If 300-800 -->
osmotic diuretic or partial DI. Osmotic diuretic is differentiated from DI via excretional
osmolarity >900mOsm/day in osmotic diuretic (volume of urine in 24 X urine
osmolarity). If less--> DI. Response to desmopressin allow differentiation of central from
peripheral.
Note urine osmolarity >800 meaning good ability of kidney to concentrate urine. If less
--> osmotic effect or DI. If <300 --> for sure DI.
Complete response to desmopressin, urine osmolarity increases via 50%. If 10-50%
increases --> partial response.

Treatment
We need to correct hypernatremia in proper rate. Aggressive correction is dangerous due
to fact that rapid water shifting into neuron cells --> seizure, coma and permanent
neurologic damage. So, as in hyponatermia, rate of correction should not exceed 10-
12mEq/L/day

In Chronic hypernatremia, symptoms are less sever secondary to adaptation mechanism

of hyper-osmolar state. We need to correct in rate 10-12 mEq/ day.

The mainstay of treatment is increase water intake. we prefer water intake via oral/ NG
tube intake or infusion of 5% dextrose or quarter saline via IV

We need to calculate water deficit

water deficit = (Na-140)/ 140 X TBW (male weight X 0.6 or female weight X 0.5)

This does not help us in choosing solute or rate of infusion. So, we prefer another way via
calculating of delta Na. However, TBW in male is weight X0.5 While in female weight X
0.4 Due to fact of volume contraction
Example

70 Kg male, his Na is 164mEq/L and K=3.

We chose 5% Dextrose water infusion (contain20mEq/L of KCL)

delta Na= 20-164/ (70 x0.5 +1) = -4

We need to decrease Na from 167 to 145, so we need 3 liters of 5 dextrose water

Rate is 10-12 per day. So, give 3 liters over 24 hours

3/24 = 1/8 =0.125 L/hour --> 125 ml

Specific therapies

 In hypoveolemia hyponatremia, we give hypotonic saline (0.45% of saline) to

replenish ECF. However, in case of sever hypovolemia --> give isotonic saline to
correct hypovolemia then give isotonic saline
 In hypervolemia hypernatremia, cessation of iatrogenic cause is sufficient
 DI: typically, it does not cause hypernatremia and hypovolemia if thirst response
is intact. So, treatment if required is best targeted to resolve the cause. Supportive
therapy
o Central via giving desmopressin
o NDI is treated via low Na diet +thiazide (mild volume depletion-->
enhance proximal water and Na re-absorption)
Ca level
Ca is essential for bone formation and neuromuscular function. 99% of Ca is stored in
bone and teeth and 1% is within ECF. 50% of ECF is bound (40% to albumin and 10%
bound to anion like phosphate) while reminder (50%) is ionized (free)

Ca is balanced via

1. PTH --> increase bone resorption and increase Ca reabsorption in kidney and
finally promote conversion of 25hydroxyvitamin D3 into 1,25 dihydroxyvitamin
D3 (1,25 dihydroxycholecalciferol= calcitriol) via activation of 1,25dihydroxy
2. Calcitriol increase Ca reabsorption from intestine.

Hypercalcemia
Definition: Serum Ca >10.3mg/dl with normal serum albumin or ionized Ca>5.2mg/dl
 Mild: 10.5-11.9mg/dl
 Intermediate 12-13.9mg/dl
 High: 14mg/dl or more

Note: Significant hypercalcemia needs increase ECF Ca content and decrease ability of
renal to excrete Ca. This is why it still asymptomatic for a while till failure of
compensatory mechanism to excrete Ca in urine like volume depletion

Since total Ca level, that we measure, depends on albumin concentration, we prefer to use
ionized Ca or doing correcting equation.

Rapid elevation of Ca level --> symptoms are sever and usually neurological symptoms.
In elderely with neurologic manifestation, neurological involvement develops on lower
threshold

Causes: (90% of hypercalcemia is due to malignant causes or primary

hyperparathyrodism)

1. Primary hyperparathyrodism: most common causes in ambulatory patient. It's

more common in elderly women patient. 85% due to single parathyroid adenoma,
15% due to hyperplasia of all four glands and 1% due to parathyroid carcinoma
2. Malignancy is the most common cause of hypercalcemia in hospitalized patient.
Most common way is secreting PTHrp (bone resporption and increase renal
tubular Ca reabsorption). Second most common way is stimulation of osteoclast
(just via bone resporption). Less common way is secretion of calcitrol (bone
 resporption and increase intestinal absorption of Ca) and via ectopic PTH seen in
ovarian cancer, small and squams lung cancer

Note: 100% of hypercalcemia in hodgikin lymphoma and 1/3 of causes of

hypercalcemia in non-hodgikin lymphoma (others via PTHrp) is due to increase
production of calcitrol via expression 1 hydroxylase enzyme (convert calcidiol to
calcitrol)

3. Less common causes of hypercalcemia accounts just for 10% of cases

a. Increase of vitamin D activity via exogenous exposure to vitamin D or
increase generation of vitamin D in granulomatous disease like sarcoidosis
b. Ingestion of large quantities of Ca containing anti-acid --> hypercalcemia,
alkalosis and renal failure. It can present as acute or chronic
hypercalcemia
c. Familial hypocalciuric hypercalcemia (FHH): asymptomatic
hypercalcemia from childhood with +ve family history since it's an
autosomal dominant disease of Ca sensing receptor. We have vitamin D
deficiency causing normal to high PTH and elevation of Ca level. It's
differentiated from primary hyper parathyrodism via checking urinary Ca
level. In primary hyperparathyrodism, we have urinary Ca
>250mg/24hours, while in FHH it's <200mg/day. Moreover, in primary
parathyrodism, Ca/Cr ratio (fractional Ca) is between0.01-0.05, while in
FHH it's less than <0.01. For diagnosis, rule out renal failure and low Ca
intake. Parathyroidectomy is useless in FHH
d. Paget's disease and hyperthyrodism can cause hypercalcemia
e. Medication like thiazide (increase Ca reabsoprtion in distal tubule), lithum
and theophylline toxicity. Vitamin A toxicity can also cause
hypercalcermia
f. Miscellaneous: acromegaly, adrenal insufficiency and immobilization

Note: there is a high co-existing probability to have primary hyperparathyrodism in

patient with malignancy.
Clinical presentation
Symptoms appear if Ca level >12mg/dl and tends to be sever if hypercalcemia develops
rapidly (acute hypercalcemia)

 Most patient of primary hyper parathyrodism is asymptomatic and detected

incidentally via increase PTH and increase Ca level with urinary Ca/Cr ranges
between 0.01-.05. It can cause osteitis fibrosa cystic (brown tumor- just in 5% of
cases) if hyperparathyrodism is prolonged and increase risk of fracture.
 Renal manifestation of hypercalcemia: polyuria, polydipsia and nephrolithiasis.
This is secondary to nephrogenic DI. Moreover, it can cause renal failure (in high
level of hypercalcemia --> renal vasoconstriction and natriuresis induces volume
contraction). Chronic elevation of Ca --> Ca deposition in tubular cells
-->degeneration of tubular cells

Nephorgenic DI occurs in case of chronic hypercalcemia secondary to Ca deposition in

medulla causing tubulointerstitial injury, downregulation of aquaprotien 2 water channel
and activation of Ca sensing receptor --> decrease water reabsorption in loop of henle and
collecting duct

 GI: anorexia, vomiting, constipation and rarely pancreatitis (Ca deposition in

pancreatic duct and activation of trypsinogen). If patient has peptic ulcer with
hypercalcemia --> think of MEN I (hyperparathyrodism, zollinger ellison
syndrome and anterior pituitary adenoma
 Musculoskeletal: muscle weakness and bone pain
 Neurologic symptoms: anxiety, depression ,fatigue, confusion and coma
 Cardiac: short QT interval secondary to shortening of cardiac action potential,
bradycardia and HTN

History:
look for duration of hypercalcemia, presence or absence of symptoms and ask for signs
of malignancy (always precedes hypercalcemia symptoms), family history and
medication. If hypercalcemia lasts longer than 6 months without symptoms --> most
likely primary hyperparathyrodism
Laboratory test
 Corrected Ca= Ca +0.8 X(4- albumin concentration)
 Serum PTH:
o If it's normal to high --> primary hyperparathyrodism. Because 20% of
primary hyperparathyrodism have normal PTH (Not low). In 20% of
primary hyperparathyrodism, we also should think of familial
hypocalciuric hypercalcemia via checking fractional Ca.
o If PTH is suppressed --> check for PTH related peptide and check for
calcitrol. Increase Calcitrol in granulomatous disease, calcitrol overdose
and primary hyperparathyrodism and acromegaly
 Serum phosphorus: if it was increase with hypercalcemia --> vitamin D
intoxication (check for vitamin D metabolites) or paget's disease. Low occurs in
both malignant and primary hyperparathyrodism because PTH enhances renal
phosphate elimination
 Urine Ca: elevated in primary hyperparathyrodism due to filtered dose of Ca
exceeds ability to reabsorb Ca. Low in thiazide medication, milk alkali syndrome
(associated with metabolic alkalosis) and FHH.
 Milk alkali syndrome: metabolic alkalosis and Cl concentration <103mEq/L.
 If all are normal --> check level of vitamin A, TSH and serum and urine protein
electrophoresis (suspect of multiple myeloma)
 ECG --> Short QT prolongation

Management
First step --> correction of hypovolemia via giving 0.9% saline patients who
demonstrate volume depletion, since hypovolemia prevents effective calciuresis (do not
forget nephrogenic DI). Euvolemia increase GFR --> enhance Ca excretion and decrease
Ca reabsorption in proximal tubule secondary to fact that saline is calciuretic

Second step: if sign of overload limit further saline administration, we give loop
diuretics. These decrease Ca reabsorption in ascending loop of henle and enhance Ca
excretion. They should not be used in euvolemic or hypovolemic state.

If saline can not solve problem and we can not give loop diuretics or given without
improvement --> give IV bisphosphenate (decrease bone resorption --> decrease Ca
level). Hydration should precede bisphosphenate use. They have a delayed response
usually after 2 days. We can give pamidronate or more potent drug like zoledronate.
After infusion, we may develop hypocalcemia after 2 days and resolves spontaneously
within 2 weeks. Relative CI is renal failure
Gallium nitrate IV same as bisphosphenate in mode of action and time of onset. Problem
is that it's CI if Cr>2.5mg/dl due to nephrotoxic effect

In case of renal failure, we prefer giving Calcitonin, which inhibits bone resorption and it
has analgesic effect especially if metastasis to skeletal muscle is the cause of
hypercalcemia

Steroid is used in management of hypercalcemia if hematoligcal malignancy (lymphoma)

and granulomatous induce production of calcitrol

Dialysis using low Ca dialysate is used in case of sever hypercalcemia (>16mg/dl) and in
patient with renal failure
Chronic management of hypercalcemia

1. Primary hyperparathyrodism --> parathyrodictomy with success rate 95% . We

detect hyperfunction gland via sestamibi (absorb more Tc99m). It's indicated in
case of
o Urinary Ca> 400mg/day
o Ca 1mg/dl more than upper limit
o Reduced bone mass T score </= 2.5
o Age <50
o Unfeasibility to follow up

If there is no indication for surgery, we should give medication like liberal oral
hydration, high salty diet and daily exercise to decrease bone resorption. You have to
avoid thiazide. In post-menopause women, we can use estrogen replacement therapy or
selective estrogen raloxifene.

2. Malignant hypercalcemia: oral bisphosphenate +steroid can be tried with

restricted Ca diet (<400mg/day).

Notes about malignant hypercalcemia

 Presence of hypercalcemia in malignancy is a poor prognostic factor.

 malignant hypercalcemia induce dehydration via hypercalcemia and nausea and
vomiting
 Treatment first via elimination of Ca from diet. The problem is development of
hypophosphatemia secondary to saline infusion, loop diuretic and PTHrP. We
need to give phosphate in diet
Hypocalcemia
Serum Ca level <8.4 with normal albumin level or ionized Ca <4.2 mg/dl

D/Dx
 Pseudo-hypocalcemia: total Ca level is decreased due to hypo-albuminemia.
However, corrected Ca level is normal
 Effective hypothyrodism:
o Acquired: more common due to infiltration or auto-immune destruction. It
can be iatrogenic post -thyroidectomy. Hypomagnesemia (<1mg/dl) or
sever hypermagnesemia (>6 mg/dl) --> decrease PTH release.
o Congenital: DiGeorge syndrome or familial hypocalcemia
 Vitamin D deficiency : mild -moderate sever --> normal Ca level due to
compensatory mechanism of increase PTH release. Sever vitamin D deficiency
--> liver cirrhosis, nephrotic syndrome, elderly people or limited sun exposure.
 Profound elevation of phosphate level --> bind Ca and precipitate into body tissue
 Alkalemia --> increase ability of Ca to bind albumin
 Post-transfusion hypocalcemia --> due to binding of Ca to citrate containing
blood product
 Ca can bind fluroquinolones

Presentation:
It depends on rate and level of Ca

 Acute moderate hypocalcemia -->increase excitability of neurons and muscle

-->distal parasthesia and tetany. Presence of chvostek and Trousseau's sign called
latent tetany
o Chvostek sign: twitching of facial muscle when facial nerve is tapped
anterior to ear lobe
o Trousseua's sign: inflate blood pressure cuff above systolic pressure for 3
minutes--> carpal spasm
 Acute sever hypocalcemia laryngospasm, confusion, seizures, or vascular collapse
with bradycardia and decompensated heart failure
Diagnosis
 First step: check albumin level to calculate corrected Ca level
 Then, check PTH,
o if low or even normal in hypocalcemia setting --> hypo-parathyrodism
either congenital or acquired.
o If high --> vitamin D deficiency, PTH resistance or hyper-phosphatemia.
 To differentiate between vitamin D deficiency and hyper-phosphatemia, we check
PO4 level. In vitamin D deficiency --> both Ca and PO4 are low.
 Measure calcidol (25 hydroxylase activity) not calcitrol since it can be normalized
via secondary increase PTH and increase 1 hydroxylase activity
 Rule out hypo or sever hyper-magnesemia in all true hypocalcaemia cases.

Do not forget hypercalcemia--> long QT interval

Treatment
Acute management of symptomatic hypocalcemia requires prompt and aggressive
therapy

 In case of hyperphosphatemia, if we give Ca --> increase Ca-PO4 deposition to

tissue --> worsening of the disease. So, we need to do dialysis ASAP. If it was
asymptomatic, decrease PO4 level prior giving Ca level.
 Hypomagnesemia: if present --> treat prior giving Ca. Give 2gram of Mg over 15
minutes
 Give Ca supplement firstly after ruling out hypomagnesemia and
hyperphosphatemia. We prefer giving Ca gluconate (not Ca chloride due to
reduced risk of tissue toxicity with extravasation). Do not forget rule of 10: give
10 ml of 10% solution (100mg of Ca gluconate per ml) over 10 minutes. So, in
one ampule (10ml), we will give 1000mg of Ca gluconate and 90mg of elemental
Ca.
 In sever hypocalcemia, we can give two ampules

 The effect of initial treatment is only transient, and maintenance of calcium levels
typically requires a continuous infusion of 0.5 to 1.5 mg/kg/hr of elemental
calcium. solution comprised of 1 L D5W with 100 mL of 10% calcium gluconate
contains ~900 mg of elemental calcium per liter, approximating 1 mg of
elemental calcium per mL of fluid. Infusion is typically begun at a rate of 50
mL/hr (~50 mg of elemental calcium per hour) and titrated up as needed.
Chronic management
 We need Ca supplements and vitamin D metabolities
o Oral Ca supplement: Ca carbonate (40% of elemental Ca) or Ca acetate
(25% of elemental Ca) can be given with goal 1-2 g of elemental Ca PO
tid
o Vitamin D supplement

Complication of treatment is development of hypercalcemia. In this case, stop Ca and

Vitamin D supplements
Phosphorus
It's critical for bone formation and energy metabolism. 85% is stored in bones and most
of remainders in the cells. So, serum phosphate does not reflect PO4 level in body

PO4 level is determined via

 PTH: it decrease renal reabsorption of PO4 --> decrease PO4

 Its own concentration regulate amount of reabsorption in proximal tubules
 Calcitrol: increase PO4 reabsorption in GI--> increase PO4
 Insulin --> decrease PO4 via shifting PO4 into cells

Hyperphosphatemia
Level of PO4 >4.5mg/dl

D/Dx
 Trans-cellular shift occurs in rhabdomyolysis, tumor lysis syndrome and massive
hemolysis. This cause release of PO4 out of cells. Hypoinsulinemia or metabolic
acidosis --> decrease PO4 influx into cells
 Increase intake: especially in case of renal failure
 Decrease renal excretion: in renal failure, pseudohypo-parathyrodism and
hypoparthyrodism

Presentation:
Hypocalcemia is due to intra-vascular chleation of Ca via PO4 through precipitation into
tissue.

It's due to hypocalcemia and metastasis calcification of soft tissue. For example,
precipitation of Ca-PO4 in skin --> pruritis

Calciphylaxis describes the tissue ischemia that may result from the calcification of
smaller blood vessels and their subsequent thrombosis

Chronic hyperphosphatemia --> renal osteodystrophy

Treatment via restoration of renal function via giving saline or acetozolamide. If renal
failure is irreversible --> hemodialysis

Chronic hyperphosphatemia is almost always associated with chronic renal

insufficiency. Its management consists of reducing phosphorus intake through dietary
modification and the use of phosphate binders

Sterwart's approach to acid base balance

Hydrogen ion is expressed via

 [H+]  =  K  x   PCO2/[HCO3-], which K is a dissociation constant. Classicaly, it's used

to interprete the acid base balance.

However, anesthesiologist and critical care professional prefer to use Stewart's approach
for acid base balance (also called strong ion difference)

Stewart's says that acidosis occurs in case of shifting of water to make more H and less
OH. He says that HCO3 is dependant variable and it's not a determinant of blood PH.

It's a quantitative way for metabolic acidosis or alkalosis

The dependant factor for acid base balances are

1. Strong ion difference (SID): Since not all ion concentration can be measured, we
say apparent SID (SIDapp). It's calculated via difference of major cation and
major anion

[Na]+ [K]+ [Ca]+ [Mg]- [Cl]- [lactic acid]

2. Plasma concentration of non-volatile weak acid (ATot). Weak acid appear in

blood either as dissociated (A-) or bound with proton (AH). ATot= [A] + [AH].
ATOt act as a buffer. In healthy, A equals phosphate, while AH equals ion
equivalence of albumin.
3. PaCO2
Since acid base balance depends on these mentioned ions. We have 6 different case
scenraios:

 Respiratory acidosis and alkalosis

 SID acidosis and alkalosis
 ATot acidosis or alkalosis

SIDapp under normal condition is 40 mEq/L. If difference >40 --> alkalosis and <40 -->
acidosis. For example, in vomiting, we have increase SID secondary to loss of Cl -->
alkalosis (Stewart think alkalosis is secondary to loss of Cl not loss of H) !! Moreover,
giving solution that has high concentration of Cl --> acidosis (gaining of Cl, not due to
dilution of HCO3).

If we do not have all of ion, we can measure Na and Cl. Difference should be 38 If more
--> alkalosis, if lower --> acidosis. Compare with base deficit, if there is difference -->
attribuated to lactate, Ca or Mg level

Since SIDapp is the function of PH and non-volatile weak acids. We can measure
effective SID based on these data.

SIDapp -effective SID should be zero. if it was +ve --> organic acid accumlation is the
cause of acidosis

effective SID(SIDeff) equals (12.2 × Pco 2 /10 -pH ) + 10 × [Albumin × (0.123 × pH –

0.631)] + [PO 4  × (0.309 × pH – 0.469)]

Since it's complex, there is equation for calculating it. Moreover, some devices measure
it. Value differ from one device to another --> this is why tradition way is still preferred

The major difference between stewart approach and traditional one is inclusion of
albumin serum in Stewart.

Metabolic alkalosis
We have an increase HCO3, PH and PaCO2. Expected PaCO2 is 40 + 0.6 x HCO3
differences.

To develop, we need initial cause and maintenance phase.

Initial cause is either vomiting, NG suction and diuretic use. Moreover, Cushing, Conn's
and Barrter's syndrome.

Maintenance cause can be due to renal hypo-perfusion --> can not get rid of H. So, it's
called saline responsive. However, maintenance issue in other causes is pathological
procress like Cushing, conn's and barrter's syndrome. In latter, Cl >20mEq/L due to
increase renal perfusion secondary to volume expansion. So, saline will not solve the
problem

saline resistance --> hypertensive (hyper-aldestronism either primary or secondary) or

normotensive --> barrter syndrome