Body fluids and fluid therapy

Body fluids and fluid therapy

AgeHeart rate

Respiratory rate

Newborn to 1 year old140401 to 4 years old120304 to 12 years old10020>12 years old8015The minimum systolic blood pressures for age are:

Newborns to 1 month old: >60 mmHg

b) 1 month old-1 year old: >70 mmHg

c) > 1 years old: (Age X 2) + 70 mmHgSkin pinch Goes back immediately in no dehydration< 2 secs some>2 secs severe

Plan A home based fluids, ORS packets

Plan BRehydration therapy : 75 ml/ kg ORS in first 4 hoursMaintenance therapy : 10-20 ml/ kg for each liquid stool

Plan C100 ml/ kg of Ringer Lactate

30 ml/kg in 30 mins + 70 ml/ kg in 2.5 hours in 1-5 years

30 ml/kg in 1 hr + 70 ml/ kg in 5 hours in 6% in an older child or adult): Peripheral pulses either rapid and weak or absent; decreased blood pressure; no urine output; very sunken eyes and fontanel; no tears; parched mucous membranes; delayed elasticity (poor skin turgor); very delayed capillary refill (>3sec); cold and mottled; limp, depressed consciousness

Correction of hyponatremic dehydration : An overly rapid (>12mEq/L over the first 24hr) or overcorrection in the serum sodium concentration (>135mEq/L) is associated with an increased risk of central pontine myelinolysis

Seizures are the most common manifestation of cerebral edema from an overly rapid decrease of the serum sodium concentration during correction of hypernatremic dehydration.Metabolic acidosis:pH > 7.2 RLpH < 7.2 NaHCO3

Late metabolic acidosis:in healthy premature infants, more chance if fed on cows milkhyperchloremic acidosisInacute respiratory alkalosis, the bicarb won't have decreased much(since the compensatory metabolic acidosis takes a few days to develop) whereas inchronic respiratory alkalosisthe compensatory metabolic acidosis will be complete and will significantly decrease the bicarb.Calculate(24- bicarb) / (40 - PaCO2)InterpretationForacute respiratory alkalosis= 0.2Forchronic respiratory alkalosis= 0.4-0.5Rule 1 : The 1 for 10 Rule for Acute Respiratory AcidosisThe [HCO3] will increase by 1 mmol/l for every 10 mmHg elevation in pCO2above 40 mmHg.Expected [HCO3] = 24 + { (Actual pCO2- 40) / 10 }Comment:The increase in CO2shifts the equilibrium between CO2and HCO3to result in an acute increase in HCO3. This is a simple physicochemical event and occurs almost immediately.Example: A patient with an acute respiratory acidosis (pCO260mmHg) has an actual [HCO3] of 31mmol/l. Theexpected [HCO3]for this acute elevation of pCO2is 24 + 2 = 26mmol/l. The actual measured value is higher than this indicating that a metabolic alkalosis must also be present.

Rule 2:The 4 for 10 Rule for Chronic Respiratory AcidosisThe [HCO3] will increase by 4 mmol/l for every 10 mmHg elevation in pCO2 above 40mmHg.

Expected [HCO3] = 24 + 4 { (Actual pCO2 - 40) / 10}Comment:With chronic acidosis, the kidneys respond by retaining HCO3, that is, renal compensation occurs. This takes a few days to reach its maximal value.Example: A patient with a chronic respiratory acidosis (pCO2 60mmHg) has an actual [HCO3] of 31mmol/l. The expected [HCO3] for this chronic elevation of pCO2 is 24 + 8 = 32mmol/l. The actual measured value is extremely close to this so renal compensation is maximal and there is no evidence indicating a second acid-base disorder.

Rule 3: The 2 for 10 Rule for Acute Respiratory AlkalosisThe [HCO3] will decrease by 2 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg.Expected [HCO3] = 24 - 2 { ( 40 - Actual pCO2) / 10 }Comment: In practice, this acute physicochemical change rarely results in a [HCO3] of less than about 18 mmol/s. (After all there is a limit to how low pCO2 can fall as negative values are not possible!) So a [HCO3] of less than 18 mmol/l indicates a coexisting metabolic acidosis.

Rule 4: The 5 for 10 Rule for a Chronic Respiratory AlkalosisThe [HCO3] will decrease by 5 mmol/l for every 10 mmHg decrease in pCO2 below 40 mmHg.Expected [HCO3] = 24 - 5 { ( 40 - Actual pCO2 ) / 10 } ( range: +/- 2)Comments:It takes 2 to 3 days to reach maximal renal compensationThelimit of compensationis a [HCO3] of about 12 to 15 mmol/l

Rule 5 : The One & a Half plus 8 Rule - for a Metabolic AcidosisThe expected pCO2 (in mmHg) is calculated from the following formula:Expected pCO2 = 1.5 x [HCO3] + 8 (range: +/- 2)Comments:Maximal compensation may take 12-24 hours to reachThelimit of compensationis a pCO2 of about 10 mmHgHypoxia can increase the amount of peripheral chemoreceptor stimulationExample:A patient with a metabolic acidosis ([HCO3] 14mmol/l) has an actual pCO2 of 30mmHg. The expected pCO2 is (1.5 x 14 + 8) which is 29mmHg. This basically matches the actual value of 30 so compensation is maximal and there is no evidence of a respiratory acid-base disorder (provided that sufficient time has passed for the compensation to have reached this maximal value). If the actual pCO2 was 45mmHg and the expected was 29mmHg, then this difference (45-29) would indicate the presence of a respiratory acidosis and indicate its magnitude. SeeSection 5.5for more details.

Rule 6 : The Point Seven plus Twenty Rule - for a Metabolic AlkalosisThe expected pCO2(in mmHg) is calculated from the following formula:Expected pCO2 = 0.7 [HCO3] + 20 (range: +/- 5)Comment:The variation in pCO2 predicted by this equation is relatively large. (The reasons for this are discussed insection 7.5)

Sodium deficit = (desired sodium present sodium) * wt * 0.6

Hypernatremia brain hemorrhage Rapid correction brain edema

Rapid correction of hypo Na

disequilibrium syndromeduring hemodialysis, when the decrease in extracellular urea is so rapid that the intracellular urea does not have time to equilibrate. This may lead to the disequilibrium syndrome, in which water shifts into brain cells, potentially causing severe symptoms.SIADH Rx: demelocycline, chronic furosemide + Na

Conivaptan V2 receptor antagonist for SIADH

Pseudohypoaldosteronism type II, an autosomal recessive disorder also known as Gordon syndrome, is a unique cause of hyperkalemic RTA because the genetic defect causes volume expansion and hypertension.

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (Michelis-Castrillo syndrome), an autosomal recessive disorder, is due to mutations in the gene for claudin 16 (paracellin-1), which is located in the tight junctions of the TAL of the loop of Henle.

Patients with familial tumoral calcinosis, a rare autosomal recessive disorder, have hyperphosphatemia due to decreased renal phosphate excretion and heterotopic calcifications.

The disease may be secondary to mutations in the genes for a glycosyltransferase, the phosphatonin FGF-23, or the gene for Klotho, which encodes the co-receptor for FGF-23.Rhabdomyolysis is the most common complication of acute hypophosphatemia, usually in the setting of an acute transcellular shift of phosphorus into cells in a child with chronic phosphorus depletion (anorexia nervosa).

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