Kebutuhan Cairan

 Perkiraan kebutuhan per hari (sehat):

 weight (30-40ml/kg/day)
 body surface area (1.5L/meter2/day)
 metabolic rate (100ml/100kcal)
Distribusi Cairan dalam Tubuh
 Tujuan Terapi Cairan IV

Resusitasi

Redistribution
4R Rumatan

Replacement

https://www.ncbi.nlm.nih.gov/books/NBK333103/
 Evaluasi hipovolemi ?
 Indikator untuk resusitasi cairan :
 SBP <100 mmHg
 HR > 90x/min
 CRT > 2 sec atau akral dingin
 NEWS skor ≥ 5
 Evaluasi  ps butuh cairan & elektrolit 
 Anamnesa : previous limited intake, thirst, the quantity and
composition of abnormal losses, any comorbidities (including
patients  malnourished - at risk of refeeding syndrome)
 PF : pulse, blood pressure, capillary refill and jugular venous
pressure o presence of pulmonary or peripheral oedema o presence
of postural hypotension
 Clinical monitoring: NEWS, fluid balance charts , weight.
 Lab : full blood count o urea, creatinine and electrolytes.
 Jenis cairan

1. Asering
 (mEq/L) Na 130; Cl 109; Ca 3 ; K 4 ; Asetat 28
2. Kristaloid
 Normal Saline
 (mmol/L) Na: 154 ; Cl:154
 Ringer Laktat
 (mmol/100 ml : Na = 130, K = 4-5, Ca = 2-3, Cl = 109-
110, Basa = 28-30 mEq /L)
 Dextrose
 Ringer asetat
3. Koloid
 Albumin
 Hidroxyetyl Starches (HES)
 Dextran
 Gelatin
 Hiponatremia

 Serum na <135 mEq/L (135 mmol/L)

 Mild (130-135)  asymptomatic
 Mild symptoms : nausea and malaise progress to headache,
lethargy, and disorientation drops.
 The most serious symptoms :
 Respiratory arrest, seizure, coma, permanent brain
damage, brainstem herniation, and death.
 Laboratory assessment : serum electrolytes, creatinine, and
osmolality ; urine sodium.
 SIADH

 SlADH is a clinical diagnosis characterized by :

(1) hyponatremia;
(2) decreased osmolality (less than 280 mOsm/kg
[280 mmol/kg] )
(3) absence of heart, kidney, or liver disease;
(4) normal thyroid and adrenal function
(5) urine sodium usually over 20 mEq/L.

 may have:
 low blood urea nitrogen (BUN) (less than 10 mg/dL [3.6 mmol/L] )
 hypouricemia (less than 4 mg/dL [238 mcmol/L] )
 The most serious complication :
 Iatrogenic cerebral osmotic demyelination (from
overly rapid sodium correction)
 Also called central pontine myelinolysis,
 may occur outside the brainstem.
 Hypoxic episodes during hyponatremia may contribute to
demyelination.
 The neurologic effects are generally catastrophic and
irreversible.
 Treatment

 Hypovolemic  adequate fluid resuscitation from

isotonic fluids
 normal saline or lactated Ringer solution
 suppress the hypovolemic stimulus for ADH release.
 Hypervolemic  loop diuretics or dialysis, or both,
 To correct increased total body water and sodium.

 Euvolemic  may respond to free water restriction

alone.
 calculate the sodium deficit and deliver 3%
hypertonic saline
 Sodium deficit = TBW x (Desired serum Na-Actual serum
Na)
 TBW  Female 50% ; male 55%
 3% hypertonic saline  sodium : 513 mEq/L

 Delivery rate = Sodium deficit/(513 mEq/L)/ 24hours

 rateshould be approx 0.25 mL/kgBB/h
 should not > 0.5 mL/kgBB/h
 Guidelines (2014)  consensus recommendations:
 serum sodium increase: 4-6 mEq/L may reverse the
neurologic manifestations of symptomatic
hyponatremia.
 acute hyponatremia (eg, exercise-associated
hyponatremia) w/ severe neurologic manifestations
 100 mL of 3% hypertonic saline infused over 10 minutes
(repeated twice as necessary)
 correction rates for chronic hyponatremia are low
 (4-8 mEq/L per 24 hours in patients at high risk for
demyelination)
 koreksi cepat:
 Acute (< 120 mEq/L symptomatik), (< 110 mEq/L)
 Mencegah edema otak atau memperbaiki edema otak
 Symptomatic Hyponatremia (Seizures, coma, etc.)
 Terapi symptoms
 3% NS, 1-2 mEq/L/h sampai:
 Symptoms membaik
 Selama 2-3 jam atau Na serum mencapai 120 mEq/L

 Koreksi lambat
 0.5 mEq/L/h with 0.9% NS
 restriksi cairan
 Lama koreksi 24 jam < 10-12 mEq/L/d  mencegah myelinolysis
 Hipernatremia

 Hypernatremia is defined as a sodium concentration

>145 mEq/L
 Typical findings: dehydrated, orthostatic
hypotension, oliguria
 Early signs: lethargy, irritability, weakness
 Severe hypernatremia (>158 mEq/L):
 Hyperthermia, delirium, seizures, coma
 Laboratory Findings:
1. Urine osmolality greater than 400 mOsm/kg  Renal
water-conserving ability is functioning.
 NONRENAL LOSSES-
 water intake < fluid losses
 from excessive sweating, the respiratory tract, or bowel movements.
Lactulose  osmotic diarrhea
 RENAL LOSSES-
 progressive volume depletion from glucosuria
 Osmotic diuresis can occur with the use of mannitol or urea.

2. Urine osmolality less than 250 mOsm/kg

 common causes : nephrogenic DI, interstitial nephritis,
hypercalcemia, and hypokalemia .
 Treatment

 correcting the cause of the fluid loss, replacing water,

and replacing electrolytes (as needed)
 increases in plasma osmolality  brain cells
synthesize solutes : ‘idiogenic osmoles’ 
intracellular fluid shifts.
 Osmole production begins 4-6 hours after dehydration and
takes several days to reach steady state.
 rapidly corrected  osmotic imbalance  cerebral
edema ; severe neurologic impairment.
 Fluids should be administered over a 48 -hour period,
 correction of approx. 1 mEq/L/h (1 mmol/L/h).
 Choice of Type of Fluid for Replacement
 Hypernatremia w/ hypovolemia
 isotonic 0.9% normal saline
 After adequate volume resuscitation  0.45% saline or 5%
dextrose (or both) can be used to replace any remaining free
water deficit.
 Hypernatremia w/euvolemia
 intravenous 5% dextrose

 Hypernatremia with hypervolemia

 5% dextrose solution
 Loop diuretics may be necessary to promote natriuresis and lower
total body sodium.
 In severe cases w/ kidney disease,  hemodialysis
 TBW = 60% x BB
 Contoh : wanita berumur 58 th BB 53 kg, diagnosis Contusio Cerebri
berat. sopor, turgor kulit turun, TD 90/60 mmhg, Na 158 mmol/l, K 4
mmol/l,
 Hipokalemia

 Serum potassium level <3,5 m Eq/L (3,5 mmo i/L)

 Severe hypokalemia may induce
 Dangerous arrhythmias and rhabdomyolysis

 Etiology:
 insufficient dietary, extrarenal or renal potassium loss

 intracellular shifting of potassium from the extracellular

space
 Cellular uptake ↑: insulin and beta-adrenergic stimulation
 The most common cause (developing countries) : gastrointestinal
loss e/ infectious diarrhea.
 mild – moderate: Muscular weakness, fatigue, and
muscle cramps
 Gastrointestinal smooth muscle involvement 
constipation or ileus.
 severe hypokalemia (less than 2 . 5 mEq/L) : Flaccid
paralysis, hyporeflexia, hypercapnia, and
rhabdomyolysis
 hypertension  clue : hypokalemia from aldosterone
or mineralocorticoid excess
 Laboratory Findings:
 Urinary potassium :
 low (less than 20 mEq/L) as a result of extrarenal loss

 high (greater than 40 mEq/L) with renal loss

 (ECG) :
 Decreased amplitude and broadening of T waves,

 prominent U waves,

 premature ventricular contractions,

 Depressed ST segments.
 Oral potassium supplementation is the safest and easiest (mild to
moderate)
 Dietary potassium  not effective in correcting potassium loss
associated with chloride depletion from
 diuretics or vomiting
 almost entirely coupled to phosphate-rather than chloride
 abnormal kidney function and mild to moderate diuretic dosage,
 20 mEq/day of oral potassium is generally sufficient to prevent hypokalemia,

 Intravenous K is indicated : severe hypokalemia and ≠ oral

 Given: up to 40 mEq/L and at rates up to 10 mEq/h.
 Concentrations of up to 20 mEq/h may be given through a central venous
catheter.
 Continuous ECG monitoring is indicated,
 serum K level  checked every 3-6 hours.
 Avoid glucose-containing fluid (prevent further shifts of potassium into the cells)
 Hiperkalemia

 Serum K level >5.0 m Eq/L (5.0 mmol/L)

 may develop in patients taking:
 ACE inhibitors, angiotensin-receptor blockers,
potassium-sparing diuretics
 Serum K : rises ±0.7 mEq/L for every ↓ 0.1 pH unit
during acidosis
 Aldosterone
 deficiency : Addison disease, chronic kidney disease (CKD)
 Resistance : genetic disorders, urinary tract obstruction
 Clinical findings:
 muscle weakness, flaccid paralysis, and ileus.

 Electrocardiography  not sensitive

 nearly half of patients  serum : >6.5 mEq/L will not manifest
ECG changes.
 bradycardia, PR interval prolongation, peaked T waves, QRS
widening, and biphasic QRS-T complexes.
 Conduction disturbances: bundle branch block, AV block

 Ventricular fibrillation and cardiac arrest.

 Hypocalcemia

 Often mistaken as a neurologic disorder.

 Check for decreased serum parathyroid hormone
(PTH), vitamin D, or magnesium levels.
 The most common cause low total ca:
hypoalbuminemia.
 Albumin <4 g/dL (40 g/L)  Ca2+ ↓ 0.8-1 mg/dL (0.20-0.25
mmoi/L) for every 1 g/dL (10 g/L) of albumin.
 Hypocalcemia : ↑excitation nerve & muscle cells
neuromuscular and cardiovascular
 Spasm of skeletal muscle
 Laryngospasm ; stridor  obstruct the airway.
 Convulsions, perioral and peripheral paresthesias,
and abdominal pain
 Classic physical findings
 Chvostek sign (contraction of the facial muscle in response to
tapping the facial nerve)
 Trousseau sign (carpal spasm occurring with occlusion of the
brachial artery by a blood pressure cuff) .
 Lab findings:
 Serum calcium : <8.5 mg/dL (2.1 mmol/L).
 Ionized serum calcium : <4.6 mg/dL (1.15 mmol/L)
 Treatment

 Severe, Symptomatic Hypocalcemia:

 10-15 mg Ca/kgBB + 1L D5W  infused over 4-6hours

 or 6-8 vials 10-mL of 10% calcium gluconate (558-744 mg of

calcium), + 1 L of D5W
 monitoring the serum calcium level : every 4-6 h

 Asymptomatic Hypocalcemia
 Oral calcium ( 1 -2 g) + vitamin D preparations

 check of urinary calcium excretion  prevent kidney fx

impairment:
 Hypercalciuria (>300 mg or 7.5 mmol/day)
 urine calcium:creatinine ratio >0.3
 Hypercalcemia

 The most common cause:

 hyperparathyroidism
 Most often asymptomatic

 Mild : ≥10.5 mg/dL

 Malignancy
 Symptomatic  usually occur serum > 12 mg/dL (3 mmol/L)

 Severe (≥14 mg/dL)

 Symptoms: constipation, polyuria, nausea, vomiting,
anorexia, peptic ulcer disease, renal colic, and
hematuria from nephrolithiasis

 Neurologic manifestations : mild drowsiness,

weakness, depression, lethargy, stupor, and coma.

 Treatment:
 Biphophonate (full tx effect : up to 48-72h)  calcitonin (short
term)
 Emergency: dialysis
 Hypophosphatemia

 Acute, severe hypophosphatemia (less than 1 .0

mg/dL [0.32 mmol/L] ) can lead to rhabdomyolysis,
paresthesias, and encephalopathy (irritability,
confusion, dysarthria, seizures, and coma).

 severe, symptomatic hypophosphatemia (less than 1

mg/dL [0.32 mmol/L] ) , an infusion : 279-310
mg/12h (or 9-10 mmol/12 h)

 Monitoring : phosphate, Ca, K every 6

 Response to phosphate supplementation is not predictable.
 Hypomagnesemia

 Magnesium oxide, 250-500 mg PO 1-2 x/day,

 For chronic hypomagnesemia.

 Symptomatic hypomagnesemia
 IV Mg sulfate 1-2g over 5-60 min + D5W or 0,9% normal
saline

 Torsades de pointes  1 -2 g of Mg sulfate + 10mL

D5W over 15 min

 Severe, non-life-threatening
 treated at a rate to 1 -2 g/h over 3 - 6 hours.