dr Iyan Darmawan

Patient was admitted 24 hours ago with loss of consciousness and hemiparesis of face and upper extremity several hours before admission. D/ Acute ischemic stroke.

PE : stupor, BP 180/110, 37oC, HR 112, RR 12 shallow breathing

Electrolyte/metabolic panelABG : PCO2 48 , PO2 90, pH 7.2

145 87

3 32

22

0.8

240

1. Is this patient dehydrated?2. Any electrolyte disorder?3. What acid-base disorder in this patient? Can we administer Meylon?4. How should neurologist handle the hyperglycemia? 5. Can Aminofluid be given at this stage?

1. Yes. The patient was dehydrated. How do I know? First, ratio of BUN / creatinine> 20 indicated dehydration. Second, serum osmolarity in this patients was as high as 2 x [Na +] + glu / 18 = 2 x 145 + 240/18 = 290 + 13.33 = 303.33. Hiperosmolarity is defined as osmolarity > 296 mosm / L. It is an indicator of dehydration

2. Patients experienced mild hypokalemia. Hypokalemia is common in stroke patients

3. The patient experienced respiratory acidosis (PCO2 48 Torr. Normal 40) with a compensatory increase in bicarbonate 32 (Normal 22-26 mmol / L). Meylon not be given to patients with respiratory acidosis, because it can be harmful and cause intracellular acidosis.

4. Hyperglycemia in patients with stroke after passing 24 hours should be regulated by insulin. GDP> 140 mg / dl or random> 180 mg / dl should be corrected until stabilized at 150 mg / dl. Parenteral glucose can be given after a blood sugar of 150 mg / dl but need the addition of insulin, 1 U per 10 g of glucose. If 1 L Aminofluid is administered (75 g glucose) it is necessary to increase insulin regular (drip) by 7.5 units, preferably separately by a syringe pump.

5. How to know whether hyperglycemia here is due to reactive hyperglycemia or diabetes exist before a stroke? Check HbA1c. If> 7% means no DM and patients require insulin dose fixed, ie, basal + prandial. The dose of insulin on DM 0.3-0.5 U / kg / day. TDDI basal dose 40% (total daily dose of insulin)

145 87

3 32

22

0.8

240

Dehydration in Stroke• Of 2591 patients registered, 1606 (62%) were

dehydrated at some point during their admission. • Independent risk factors for dehydration included older

age, female gender, total anterior circulation syndrome, and prescribed diuretics (all P<0.001).

• Patients with dehydration were significantly more likely be dead or dependent at hospital discharge than those without (χ2=170.5; degrees of freedom=2; P<0.0001).

Dehydration in Hospital-Admitted Stroke Patients: Detection, Frequency, and Association Stroke (2012) 43(3): 857-859

• Hemodynamic status?• Cardiovascular and renal function?• Degree of dehydration?• Electrolyte status?• Acid-base?• Comorbidity?

PhysiologicalFluid Choice

Most patients get empiric fluid therapy(Isotonic solution for replacement and maintenance solution

for hemodynamically stable patients)

Ideally Fluid therapy should be tailor-made

Hemodynamic Disturbance(Shock)?

MAP < 65 mmHgTachycardiaCold extremitiesCRT > 2 seconds

Yes No

RESUSCITATION Electrolyte/Metabolic Disturbance?

ASERING

Lactated Ringer’s Yes No

Normal Saline

Colloid Malnourished?

CorrectedNaCl 3%KAEN4A Yes No

KCl 7.46%

Meylon PPN Maintenance

MgCl 20% Amiparen Aminofluid

Insulin Aminovel KAEN3B/3A

Glukosa 40% KAENMG3 KAEN 4A/4B

Lipid

InsulinCatecholamine

ADH(AVP)Aldosterone

Renalfunction

IV

Fluid &Electrolyte

status

Drugs

TraumaInfectionsepsis

Intake &excretion

Conditions of Acute Stroke

• Dehydration• Hyperglycemia• Inadequate oral intake, dysphagia• Electrolyte disorders: HypoK+, HypoNa+

Electrolyte Composition

mEq/L

Na+

K+

Ca2+

Mg2+

Cl-

HCO3-

HPO42-

SO42-

Organic Acid

Protein Total

Total

Extracellular Fluid IntracellularFluidPlasma Interstisial

453

154

14442.51.5

152

15150

227

194

27215

16154

11430

2150

152

110

10020

63194

103

142

CationAnion K+ Mg2+

HPO42-

Na+

Cl-

Predominant ions in ICF

Predominant ions in ECF

Capillary Membrane Cellular membrane

-

Terminology

• %

• mmol

• mEq

• mOsm

= g/dl

= mg/BM

MW = molecular weight

= mmol x valency

= Σ mmol solutes

e.g NaCl 0.9% = 0.9 g/dl = 9 g/L5% dextrose = 5 g/dl = 50 g/L

e.g. NaCl 9 g/L = 9 x 100023 + 35.5

= 154 mmol/L

e.g. 1.75 mmol Ca++ = 3,5 mEq

Plasma Osmolarity

• Effective Osmolality (Osmotic pressure)=2 x [Na+] + [Glu]/18

• 285 + 5 mOsm/L

Osmolalirity= 2 x [Na+] + [glucose mg/dl] + [BUN mg/dl]18 2,8

Replace acute/abnormalloss

Isotonic infusion

800 ml 200 ml

• ASERING• Lactated Ringer’s• Normal saline

1 L of

increases ECF

ICF ISF Plasma

Na+ 130 Cl- 109 K+ 4 Ca++ 3 lactate- 28

Na+ 154Cl- 154

Na+ 130 Cl- 109 K+ 4 Ca++ 3 acetate- 28

Shock + acidosis

Shock + alkalosisHyponatremia

increases ICF > ECF

ICF ISF Plasma

Replace Normal loss (IWL + urine)

Hypotonic infusion

5% dextrose/ Maintenance sol

85 ml255 ml660 ml

1 L of

increases intravascular

ICF ISF Plasma

Hemorrhagic shockBurnReserved for patientsin whom ISF expandedbut intravascular andalbumin is severelydepleted

Albumin infusion

Albumin 25%

300-600 ml over 30-60 min

100 ml L of

Ref. Evan R. Geller. Shock & Resuscitation. McGraw Hill, 1993. p 221

increases intravascular

ICF ISF Plasma

Hemorrhagic shockDSSLoading reg anes

Plasma Expander infusion

DextranGelatinHES

500 m L of

750 ml at 1 hour; 1050 ml at 2 hrRef. Evan R. Geller. Shock & Resuscitation. McGraw Hill, 1993. p 225

Electrolyte Disorders• More common in SAH, head injury than

in ischemic stroke• Hyponatremia (CSWS ; SIADH)• Hypokalemia

Hyponatremia

SIADH CSWS

Volume replacementwith saline

Fluid restrictionVasopressin antagonist, eg tolvaptan

•more common in SAH & head injury•mortality rate 15%

SIADH vs CSWSSIADH• Hematocrit N or low• Well hydrated• Avg day of

appearance 8th day• Heart rate slow/N• Urea or creatinine

N/low• GFR increased

CSWS• N or high• Dehydrated• 4-5th day• Tachycardia or N• Urea or creatinine N

or high• GFR decreased

•James Springate. Cerebral Salt-Wasting Syndrome eMedicine Journal, November 1 2001, Volume 2, Number 11 Neurosurg Clin N Am 21 (2010) 339–352

Hypernatremia•Fluid restriction, osmotic challenge•mortality rate 42%

Diabetes insipidus Iatrogenicurine output > 300 ml/hrSpec gravity < 1.003Urine osmolarity < 250

5-10 units Pitressin IV or IMDesmopressin acetate

Appropriate fluidmanagement

Hypokalemia (serum K+ < 3.4 mEq/L)

• Observational study of 421 stroke patients• More prevalent than myocardial infarction (84

[20%] vs 15[10%] ) or hypertension(84 (20%) vs 13(10%), even after patients receiving diuretics had been excluded.

• Higher risk of death• Hypokalemia in post stroke patients are common

and associated with poor outcome

Garibella SE, Robinson TG, Fotherby MD. Hypokalemia and potasssium excretion in stroke patients.J Am Geriatr Soc 1997 Dec;45(12):1454-58

Dehydration and VET after Stroke

• Serum Osmolarity >297 mOsm/kg, • Urea >7.5 mmol/l and • Urea:creatinine ratio (mmol:mmol) >80

several days post stroke was associated with odds ratios for VTE, 4.7, 2.8 dan 3.4 (p = 0.02, 0.05, 0.02) respectively using multivariable analysis

Kelly J.at al. Dehydration and VET after acute stroke. QJM, (2004) 97 (5): 293-296.

Osmolality mortality

Bhalla A. Influence of Raised Plasma Osmolality on Clinical Outcome After Acute Stroke Stroke 2000;31:2043-2048

• 167 Patients . Mean admission (300 mOsm/kg, SD 11.4), maximum (308.1 mOsm/kg, SD 17.1), and AUC (298.3 mOsm/kg, SD 11.7)

• Plasma osmolality were significantly higher in those who died compared with survivors (293.1 mOsm/kg [SD 8.2], 297.7 mOsm/kg [SD 8.7], and 291.7 mOsm/kg [SD 8.1], respectively; P<0.0001).

• Admission plasma osmolality >296 mOsm/kg was significantly associated with mortality (OR 2.4, 95% CI 1.0 to 5.9). In patients hydrated intravenously, there was no significant fall in plasma osmolality compared with patients hydrated orally (P=0.68).

Innovation is needed to improve quality of care

Role of electrolytes (cations & anions)

Electrolytes Role Conc

Na+

Cl-

HCO3-Protein

K+

Mg++

Ca++

P

Maintain extracellular osmolaroty and volume

Major extracellular anion (Na+ pair)

Maintain blood pH (pH 7,4)

Maintain circulatory volume

Nerve conduction and muscle contraction

Co-enzyme

Formation of bones and teeth, nerve conduction and muscle contractionFormation of bone and teeth, energy source(ATP)

135-145 mEq/L

97-106 mEq/L

22-26 mEq/L

6,7-8,3 g/dl

3,5-5.5 mEq/L

1,8-2,4 mg/dl

8,5-10,5 mg/dl

2,5-4,5 mg/dl

Cut-off glucose levels for intervention

• Stroke 2004;35;363-364 :(European Stroke Initiative [EUSI] guidelines 10 mmol/L, American Stroke Association [ASA] guidelines 300 mg/dL)

Adams HP,et al. Guidelines for the Early Management of Adults With Ischemic StrokeStroke. 2007;38:1655-1711A reasonable goal would be to treat those patients’ elevated glucose concentrations (140 to 180 mg/dL).

Typical Infusion Solutions

• NaCl 0.9%• Ringer’s solution• Ringer’s acetate• Ringer’s lactate• 5% Dextrose

Solutions with Na > 130 mEq/L

Na+ (mEq/L)

K+ (mEq/L)

Cl-

(mEq/L) Dextrose

(g/L)

mOsm/L)

NaCl 0,9% 154 - 154 - 308

Ringer 147 4 155,5 - 310

RL/ RA 130 4 109 - 273

Plasma 142 4 103 285 + 5

Ringer Solution is NOT RL minus lactate

Na Lactate Bicarbonate

LACTATE VS. ACETATE

Na Acetate Bicarbonate

100 mEq/hr

250-400 mEq/hr

Normal osmolality

• calculated: 2 x[Na+] + Glu/18 + urea/2.8

• 285 + 5 mOsm/L

> 296 mOsm/L hyperosmolar state

Vol of MgSO4 added into 1L Acetated Ringer’s

Current Osmolarity of DesiredAsering (Ringer’s acetate) osmolarity273.4 285 7.25

273.4 290 10.375

273.4 295 13.5

273.4 300 16.625

ml of 20% MgSO4to be added to 1L

12 mEq

17 mEq

22.41 mEq

27.5 mEq

Σ Mg

Mannitol vs HSMannitol

• Freely filtered at glomerulus, accounting for diuresis and hyponatremia

• Reduces systemic vascresistance

• Mild positive inotropic• Scavenges toxic oxygen free

radical (cytoprotection• 0.25-1.5 g/kg iv bolus• Max effect in 20-40 minutes

HS• Diureric effect via ANP• Augment intravascular volume

and cardiac performance• 1-2 ml/kg/hr• 300 ml/20 min Intracranial

pressure fell immediately after initiation of infusion with further significant decreases observed at 20 and 60 minutes (30.4 ±8.5, 24.3 ± 7.4, and 23.8 ± 8.3 mm Hg, respectively; P < .01)

1. 1ilkes GE, Whitfield PC Intracranial pressure and cerebral blood flow Surgery (Oxford), Volume 25, Issue 12, December 2007, Pages 530-5352. Wendy C. Ziai, Thomas J.K. Toung, Anish Bhardwaj Hypertonic saline: First-line therapy for cerebral edema? Journal of the Neurological Sciences,

Volume 261, Issues 1-2, 15 October 2007, Pages 157-1663. Sheng-Jean Huang, Lin Chang, Yin-Yi Han, Yuan-Chi Lee, Yong-Kwang Tu Efficacy and safety of hypertonic saline solutions in the treatment of

severe head injury Surgical Neurology, Volume 65, Issue 6, June 2006, Pages 539-546

Conclusion

• Dehydration and increased osmolarity should be managed

• Hyperglycemia(or hypoglycemia) and electgrolyte imbalances could occur (eg Hyponatremia, hypokalemia)

• Acute Phase: isotonic fluid (eg. Acetated rfinger’s, normal saline); avoid glucose

• Maintenance Phase, glucose and potassium containing solutions

Thank you