Kebutuhan Cairan

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 Asering

1. 

(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 = 109110, 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  rate

should 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) 



Symptomatic Hyponatremia (Seizures, coma, etc.) 



Mencegah edema otak atau memperbaiki edema otak 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 LOSSESwater intake < fluid losses  from excessive sweating, the respiratory tract, or bowel movements. Lactulose  osmotic diarrhea 



RENAL LOSSESprogressive volume depletion from glucosuria  Osmotic diuresis can occur with the use of mannitol or urea. 

Urine osmolality less than 250 mOsm/kg

2. 

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.