fluid and electrolyte balance in neurosurgery

7/28/2019 Fluid and Electrolyte Balance in Neurosurgery

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Presented by: Vikas Naik


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INTRODUCTIONINTRODUCTIONBody Fluid Compartments:Body Fluid Compartments:

ICF:ICF:55%~75%55%~75%

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Male (60%) > female (50%) Most concentrated in skeletal muscle TBW=0.6xBW ICF=0.4xBW ECF=0.2xBW

IntravascularIntravascular

plasmaplasma

X 50~70%X 50~70%lean body weightlean body weight

ExtravascularExtravascular

InterstitialInterstitialfluidfluid

TBWTBW

ECFECF

3/4

1/4

1/3


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Introduction

Total body water 94% weight in early

gestation

Decreases to 78% at term

eac es a u t eve s o y mont s

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INTRODUCTIONINTRODUCTIONComposition of Body Fluids:Composition of Body Fluids:

Na+

Cl-

HCO3-0

50

100

150Cations Anions

ECF

Ca +

Mg 2+

K+

PO43-

Organicanion

Protein

50

100

150

ICF

Osmolarity = solute/(solute+solvent)Osmolarity = solute/(solute+solvent)

Osmolality = solute/solvent (290~310mOsm/L)Osmolality = solute/solvent (290~310mOsm/L)

Tonicity = effective osmolalityTonicity = effective osmolality

Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)

Plasma tonicity = 2 x (Na) + (Glucose/18)Plasma tonicity = 2 x (Na) + (Glucose/18)


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Objectives of IV Therapy

Maintain daily body fluid requirements

Restore previous body fluid losses

Replace present body fluid losses


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Average daily water balance of ahealthy adult (70 kg)

Intake output

Beverage 1200ml urine -1500mlsolid food 1000ml insens.loss- 900ml

Oxidation 300ml faces -100ml


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Fever Pyrexia increases insensible lossby about 20% for each C rise in bodytemperature

Ventilator

GI losses Equivalent volume of normalsaline added with potassium chloride use tocover the gastrointestinal fluid loss and fluidsequestrated in the bowel.


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Normal volume and composition ofbody fluids


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Clinical parameters for evaluation of water balance

CVP

Pulse Peripheral Veins Wei ht

Thirst Intake and Output Skin Edema Lab Values


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Maintenance dose

For 24hrs

100ml/kg for 1-10kg

50ml/kg for 11-20

- v

or 4ml/kg/hr for 1-10kg

2ml/kg/hr for 11-201ml/kg/hr for 21-above


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Pediatric neurosurgical patients over24hrs

premature 90-100ml/kgat term 80-90ml/kg

3m-1 r 70-80ml/k

>1yr 70ml/kg


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Effect on cerebral oedema formation

Effect on CPP

Effect on glucose

Effect on electrolytes

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IV fluids divided into crystalloid and colloidde endin on molecular wei ht of solutes

crystalloids 30,000mmol


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Crystalloids:Crystalloids:

Isotonic crystalloids

- Lactated Ringers, 0.9% NaCl- only 25% remain intravascularly

- 3% NaCl

Hypotonic solutions

- D5W, 0.45% NaCl- less than 10% remain intra-

vascularly, inadequate for fluid

resuscitation


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Colloid Solutions:Colloid Solutions:

Contain high molecular weight

substancesdo not readily migrate across

capillary walls

repara onsPlasma protein fractions

Gelatins

Dextrans

Starches


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Plasma Derived Colloids

Plasma (FFP, cryoprecipitate)- Coagulation problems only

Plasma protein fraction/SHS

- Very expensive

- No proven benefit- ? harmful


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Colloids

GELATINS DEXTRANS HES

Molecular weight 28-35 kda 40-70 kda 70-450 kda

Advantages Improvescirculation

Improvescirculation

Improvescirculation,

endothelialunc on

Anaphylaxsis High small minimal

VOLUMEEFFECT

SHORT MEDIUM LONGTERM

COAGULATION +/- ++ +

DOSE

LIMITATION

NO 15ml/kg/24hr 33ml/kg/24hr


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Which Fluids ? Depends on Nature of Loss!

Balanced approach for resuscitation:

2-3 crystalloid then colloid

? 0.9% saline or HS for head injuries Ringers for other fluid resuscitation

Colloids included for major resuscitation

Blood as needed for Hct = 30


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Crystalloid

Extracellar expander

Limited volume expansion

Maintain urine output

Reduce plasma oncotic pressure Variable electrolyte content

Cheap!


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Colloid

Advantages:Intravascular expanders

Disadvantages:Coagulation problems

Variable electrol te

Rapid resuscitation

Maintain oncotic pressure

Less tissue oedemaLess pulmonary oedema

contentVariable half-life

Adverse reactions

EXPENSIVE!


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The Influence of Colloid & Crystalloid on BloodThe Influence of Colloid & Crystalloid on BloodVolume:Volume:

1000cc

200 600 1000

Lactated Ringers

Blood volume

Infusionvolume

500cc

500cc

500cc

5% Albumin

6% Hetastarch

Whole blood


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1.Should not be used except fortreatment

.

2.Solution of 5% dextrose ishypoosmolar

3.RL is also slightly hypoosmolar,administration of >3 litres canreduce

plasma osmolality.23/03/2012


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osmolality approximately that of plasma. , , . Hyperchloremic metabolic acidosis may

result with NS

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Usually Ringers lactate and/or NormalSaline

- vo ex rose u s Infusion rate should be to replace urineoutput and insensible losses ml. for ml.

Replace blood loss at 3:1 ratiocrystalloids or 1:1 of colloids downto

haematocrit of 25-30%23/03/2012


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Permissible blood loss

EBV x (HIHd ) /HI

EBV=weight x avg blood volume


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Increases plasma- cerebral parenchymaosmolality gradientdose -0.5-2.0 gm/kg

arge ose en ances cere ra ooflow and free radicalscavenging

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Mechanism of action is similar to mannitol Strengths of HS 3, 5 7.5%

causes less diuresis

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Transfusion of blood in the form of packed cell if Hb< 8

Dilutional clinical coagulopathy when blood lossexceeds more than one blood volume

Fresh frozen plasma to be administered if prothrombintime> 1.5 time normal

Dose of FFP: 10- 15 ml/ k to obtain 30% of lasma

factor concentration) Prophylactic administration contraindicated

Platelet deficiency occurs if blood loss exceeds > 1.5times EBV (14)

Transfusion indicated if counts less than 50,000/ cmmor if higher counts with bleeding

Dose of platelet concentrate- one platelet concentrateper 10 kg body weight

Use of antithrombin III controversial


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Dual set of problems

Hypovolemia

Hyponatremia- CSW and SIADH

Avoid dehydration

ere ra vasospasm y

hypervolemia by CVP of 8- 10

hemodilution by PCV around 30- 35

hypertension Avoid dextrose containing solutions

Prefer colloids for volume expansion

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ElectrolytesNormal values

Na+ - 130-149meq/l

K+ - 3.5-5meq/l

Cl- 95-110 meq/lCa- 8.1-10.4mg%


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Daily recommended amountElectrolyte Parenteral Equivalent of RDA Usual Intake

Sodium 12 meq/kg +

replacement, but

can be as low as

540 meq/d

Potassium 40100 meq/d +

replacement of

unusual lossesChloride As needed for acid-base

balance, but usually 2:1 to

1:1 with acetate

Acetate As needed for acid-base

balance

Calcium 10 meq 1020 meq/d

Magnesium 10 meq 816 meq/d

Phosphorus 30 mmol


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Factors controlling sodium Reabsorption

in Perioperative Period

RAS:- Renin secretion increases formation ofAngiotensin IIAldosterone Na reabsorption in

Distal tubule

Sympathetic nervous system- Increased

proximal tubule

ADH- it has little action on sodium excretion.,itmostly maintains extracellular fluid volume

ANP- it is released from atrial cells & causesafferent arteriolar dilation & efferent arteriolar

constriction thus increasing GFR & natriuresis


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HYPONATREMIA

Hypovolumic Hypervolumic EuvolumicCCF

NEPHROTIC SYNDROME

RENAL FAILURECIRRHOSIS

Extra renal sodium loss

diarrhea

VomitingBlood loss

Excessive sweating

Renal sodium loss

SIADHCNS

SOLTrauma

HemorrhageStrokeInflammatory

disordersdemyelination

Diuretics

Osmotic diuresis

Adrenal insufficiency

ketonuria

CarbamazepineChlorpropramidePhenothiazinesSRITCA

Pulmonary

conditionsInfectionsALINeoplasia

THIAZIDE DIURETICSHYPOTHYROIDISMADRENAL

INSUFFICIENCY


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Assesment of Pt with Hyponatremia

Clinical-

Skin turgor & mucous membranesJVP

.

daily wt.

Biochemical-

Serum Na+ & osmolarityUrine vol,S.G, Na+ & Osmolarity

BUN ,Cr,K+, Uric acid, Albumin,Cortisol


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HYPONATREMIA Contd ECG features-

Mostly non specific Appears when Na+< 115mmol/l

, ,

Bradycardia, Ventricular ectopics alsopossible

At values< 110mmol/l cardiac arrest mayoccur.

Algorithm for assesment of Hyponatremia


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Serum

Na


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Dose of Na+(meq)=wt(Kg)(140-Na+)

0.63%NS

- . -

Na=125meq/l

Half the deficit can be administered over 1st 8hrs, rest over 1-3 days

Correct underlying disorder


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Hypertonic saline - symptomatic

Fluid restriction /Normal saline -asymptomatic patients

a t rep acement

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Complication of Treatment

Pontine Myelinolysis - quadriparesis ,ataxia,abnormal extraocular movements. can occur withra id correction

Renal Failure, Peripheral edema, pulmedema, heart failure


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SIADHDiagnostic Criteria of SIADH:-summarised by

Harrigan 1996 Serum sodium serum osmolality

Normal thyroid, adrenal, renal function

Absence of peripheral edema ordehydration

Clinical features are same of hyponatremia

Specific Treatment of SIADH


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Specific Treatment of SIADH

Fluid restriction- 1 l/day. (0.9% saline is usualchoice)

Furosemide

- -,

on renal tubule

Demeclocycline -900-1200 mg in divided doses,takes 3wks for maximal effect, Induces nephrogenicDI.

Fludrocortisone -requires 1-2 wks &,retains

sodium, inhibits thirst.


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Cerebral salt wasting

syndrome

Renal loss of sodium due to intracranial

disease, leading to hyponatremia &hypovolemia

Causes: Head injury Brain tumor

Stroke Intracerebral hemorrhage Tuberculous meningitis

Craniosynostosis repair


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Cerebral salt wasting syndrome (

CSWS ) Pathophysiology not fully understood-

hypothesis

natriuretic response due to SNS overactivityand DA release causes urinary sodium loss

release - brain natriuretic peptide, C-typenatriuretic peptide or an oubain like peptide,by the injured brain

CSWS usually appears in the first week afterbrain injury and spontaneously resolves in 2-

4 weeks


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Specific Treatment of CSWS

Fluid & Sodium Resuscitation -0.9%saline used

acute s m tomatic -h onatremia 3%

NS Oral fludrocortisone - 0.1mg-0.4mg to

limit ve sodium balance in ptsrefractory to salt & fluid therapy


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Aneurysmal SAH Abnormal sodium levels seen in acute

period(4-10days) Incidence is 29%-43% Sayamaet alNeurolog res2000; 22:151-55, found

. om- -a w ypona rem aMCA-18% - a/w hyponatremia

Moringaet al -84% with hyponatremia hadsymptomatic vasospasm

Hasan et al Ann neurol 1990;27:106-180didnt finddifference in mortality rates

Possible cause of hyponatremia is release of

BNP


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Transsphenoidal surgery for Pituitary Tumors

DI is Common

CSW may commonly co-existAlbanese et al ,andrews et al Neurosurg1986;18:469-471

CSW is thou ht to occur secondaril to

release of BNP. After pituitary adenomaresection.

Triple response

-initial 4-8 day period of DI-excessive release of ADH for 14

days

-Permanent DI


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Surgery for Craniosynostosis

Frequently occurs, but usually

asymptomatic & transient

Etiology not conclusive-could be SIADH a/w large fluid shifts

CSWS has also been reported by

KappyPlastic reconstr surgery 2001;108:1501-1508


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Defined as serum Na >145mmol/l Clinical variables:

Hypernatremia

1. Body weight2. Peripheral oedema

3. CVP

4. Serum sodium/ Urine spot sodium

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Major causes of hypernatremia

CAUSES

Impaired Thirst

MECHANISMS

Coma,Essential Hypernatremia

Excessive water loss Renal

Extrarenal

Combined disorders

Mannitol, DKA, Non ketotichyperosmolar coma

Pituitary DI,Nephrogenic DI

Sweating

Coma + Hypertonic nasogastricfeeding


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Most s/s of hypernatrmia are

neurological

Altered mental status

Hypernatremia

Weakness Neuromuscular irritability

Focal neurological deficit Occasional coma/seizures


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Algorithim for assessment of Hypernatremia

Serum Na

> 145 mmol/L

Urine

Inappropriately

Urine

Appropriately

Assess urine

osmolality

Dilute concentrated

HypovolemicEuvolemic

Hypervolemic

Hypovolemic Euvolemic

Hypervolemic

Diabets Insipidus

Renal Disease

Mineralocorticoid

Excess

Extrarenal

Water loss

Iatrogenic Na

Administration

Assess volume

status

Assess volume

status


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Management of Hypernatremia Goals

Stop loss of water by T/t of cause Correct water deficit

Water deficit can be calculated as

(S Na+

-140/140)x TBW.If serum glucose is elevated, then thecorrected formula is

S Na+=S Na+

+( S glu-90)/36As in hyponatremia, rapid correction ofhypernatremia is also dangerous


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Water deficit to be corrected over 48-72 hrs No more than 0.5mmol/l/hr &12mmol/l/day

Management of Hypernatremia

u

Safest method of correction is water by

mouth or NG tube.

If patient cannot take orally, 5% Dextrose canbe given intravenously


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CENTRAL DI:-


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CENTRAL DI:

It is a failure of release of ADH fromHypothalamo-pituitary axisCharacterised by inability to concentrate

urine ,thus passage of large amount of

dilute urineRise in Plasma osmolality & progressive

dehydration

Particularly seen after pituitarysurgery,TBI, A Com Art aneurysmalSAH, & in brain death patients

*Compromise of Hypothalamic centers or the supra

optic tract above the median eminence:-permanentDI

Damage below median eminence or removal ofposterior lobe of pituitary:- transient DI


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Etiology of Central DI

Acquired Head trauma

Post-pituitary surgery

Congenital Midline craniofacial

anomalies

Holo rosence hal

Granulomas Infections

Inflammations

Chemical toxins Tetrodoxins,Snake

venoms

Vascular

Idiopathic

Ectopia of Pituitary Genetic

Autosomal dominant

Autosomal Recessive

X-linked recessive

Deletionchromosome7q


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ETIOLOGY OF NEPHROGENIC DI

Acquired

Drugs Lithium Demeclocycline

Vascular

SCD ATN

Granulomas

Amphotericin B Aminoglycoside Cisplatin Rifampicin Foscarnet

Metabolic Hypercalcemia Hypokalemia

Obstruction

Infiltrations Pregnancy IdiopathicGeneticX-linked recessive(ADH

receptor V2).Autosomal Recessive

(Aquaporin-2 gene)

Diagnosis of postoperative


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g p p

diabetes insipidus

Rule out osmotic diuresis or fluid overload

Clinical signs and symptoms

Polyuria, abrupt high volumes (4 L/day18 L/day)( within 2448 hours postoperatively)

Polydipsia, with craving for cold fluids

With/without hypovolemia

Diagnosis of postoperative


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Laboratory data

Dilute urine (specific gravity 50ml/kg+

urine osmol


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ALGORITHM FOR DIAGNOSIS OF DI

urine osmol 300mosmol/kg

Urine osmol50% Small/no increase Plasma AVP same

Severe Pituitary DI Severe nephrogenic DI Partial Nephrogenic DIPartial pituitary DI

/Primary polydipsia


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Maintenance


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Maintenance

drink according to thirst

Supplement hypotonic (D5W to D51/2NSS)

Monitor for resolution of transient DI or triphasic response

Positive daily fluid > 2 L suggests SIADH

Withhold -Antidiuretic hormone therapy

Manage anterior pituitary insufficiencystress dose -hydrocortisone 100 mg TDS


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Chlorpropramide It acts by potentiating the action of AVP or activation

of V2 raceptors Dose is 125-500mg OD

nset slow efficac less efficac can be increasedby simultaneous use of Thizides.Hypoglycemia is asignificant side effect

Clofibrate & Carbamazepine is also helpful infew patients


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Nephrogenic DI:-

T/t of cause & omitting the culprit druggenerally cures the disease

Amiloride (esp in pts. On lithium) Indomethacin

Low sodium diet


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FLUID DEPRIVATION TEST

Indication Evaluation of Diabetes InsipidusPrecautions: Requires close

monitoring

Monitor urine output Monitor vital signs

Monitor weight Do not allow weight loss to exceed

>3-5%

CONTD..

Technique


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Technique Fluid restrict patient

Mild polyuria (10 L/day) Start fluid restriction 2 hours before test

Follow Serum Osmolality to steady state

water Measure Serum Osmolality hourly until endpoint: Two values are within 30 mOsm of each other Weight loss exceeds 3-5%

Administer endogenous ADH Vasopressin 5 units Sc Intranasal DDAVP 10 ug

Measure Serum Osmolality 1 hour after ADH

administered


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Hypokalemia

Normal requirement 1meq/kg/day

Serum otassium < 3.5 mE / liter

Causes: intracellular shiftpotassium depletion

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Hypokalemia


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Transcellular shift:

beta agonists

diuretics

alkalosis

hypothermiainsulin

Potassium depletion:renal losses: diuresis/ failure

Extra renal losses: diarrhea/ NG drainage


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Clinical features hypokalemia

Muscle weakness and mental status

ECG changes prominent U waves,flattening and inversion of T waves,prolonged QT interval

Does not cause arrhythmias on its ownbut definitely is proarrythmic

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Hypokalemia


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Hypokalemia

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DiarrhoeaUrine chloride

< 15 mEq/ ltr

Urine chloride

> 15 mEq/ ltr

NG drainage

Alkalosis

Diuresis

Mg depletion

Management of hypokalemia


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Correct the primary cause

Potassium deficits in hypokalemia for 70Kg male

Serum potassium Potassium Deficit in %

3.0 175 52.5 350 10

2.0 470 15

1.5 700 201.0 875 25

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Serum potassium > 5.5 mEq/ liter

Most common cause is traumatichemolysis during venipuncture

20% blood sample incidence withelevated potassium

Source: transcellular shift ( urinary

K>30)renal cause ( urinary K< 30)

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Trans cellular shift:


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Acidosis

Rhabdomyolysis

Drugs: digitalis/ beta antagonists Renal causes:

Adrenal insufficiencyDrugs: ACE inhibitors/ B-

blockers/ cyclosporine/ digitalis/ diuretics/

heparin/ NSAIDS/ septran/ muscle relaxants Blood transfusions

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Management

Guided by serum potassium and ECGmanifestation

. evere cases - ve m - ca c um

gluconate over 5 minutes

Repeat second dose if necessary

No role for third doseAction lasts for 20 minutes

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2. Insulin dextrose: 10 U regular insulin in500 ml 20% dextrose to infuse over 1 hour-

decreases K by an average of 1 mEq/ L

3.Loop diuretics

4.Exchange resins

5.If refractory - hemodialysis

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Metabolic acidosis


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High Anion Gap

Renal failure

toxins ketoacidosis

orma an on gap

(hyperchloremic) Hyperkalemia obstructive uropathy diarrhea renal tubular acidosis

Some medications23/03/2012

Clinical features


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Headache

Drowsiness

Nausea/ vomiting/ diarrhea Kussmauls respirations

-

Hyperkalemia Hypotension

Bradycardia

GI distention

pH low (< 7.35)

HCO3 low (< 22)23/03/2012


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Management:

Fluid resuscitation

Correct underlying disorder Sodium bicarbonate only if pH< 7.20

Method: 0.5 x body weight x base deficit

correct half as slow infusion over few

minutes

other half to be repeated over 8 hours

repeat ABG values

stop when ph 7.2023/03/2012

M b li lk l i


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Metabolic alkalosis Etiology:

1.Vomiting2.Diuretics

3.Volume depletion

4.Hypokalemia

5.Organic anions like lactate

6.Chronic CO2 retention

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Metabolic alkalosis


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Clinical features

Shallow breathing Nausea/vomiting/diarrhea

on us on

Numbness / tingling

Hypocalcemia

Hypokalemia pH high (> 7.45)

HCO3 high (>26) cal features:23/03/2012

M t b li lk l i


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Metabolic alkalosis Management: saline infusion (0.2*body

weight* chloride deficit) In resistant cases give 0.1N HCl (0.5*

body weight* base excess)

Acetazolamide

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M t b li lk l i


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Management: saline infusion (0.2*body

weight* chloride deficit) In resistant cases give 0.1N HCl (0.5*

Metabolic alkalosis

body weight* base excess)

Acetazolamide

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R i t id i d lk l i


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Respiratory acidosis and alkalosis

Treatment of underlying cause

Correction of oxygenation Sedation, reassurance and CO2

rebreathing for alkalosis

Ventilatory support and chestphysiotherapy

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fluid and electrolyte balance in neurosurgery

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