fluid and electrolyte balance in neurosurgery.pdf

8/14/2019 Fluid and electrolyte balance in neurosurgery.pdf

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Presented by: Vikas Naik


2/92

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Introduction


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Introduction

Total body water 94% weight in early

gestation

Decreases to 78% at term

Reaches adult levels of 60% by 9 months

6/19/2009


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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 a

healthy adult (70 kg)

Intake outputBeverage 1200ml urine -1500ml

solid 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 of

body fluids


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Clinical parameters for evaluation of water balance

CVP

Pulse

Peripheral Veins

Weight 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

20ml/kg for 21-above

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

2ml/kg/hr for 11-20

1ml/kg/hr for 21-above


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Pediatric neurosurgical patients over

24hrs

premature 90-100ml/kg

at term 80-90ml/kg

3m-1yr 70-80ml/kg>1yr 70ml/kg


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Effect on cerebral oedema formation

Effect on CPP Effect on glucose

Effect on electrolytes

6/19/2009


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IV fluids divided into crystalloid and colloid

depending on molecular weight of solutes

crystalloids 30,000mmol


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(+//+1,


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Plasma Derived Colloids

Plasma (FFP, cryoprecipitate)

- Coagulation problems only

Albumin

Plasma protein fraction/SHS

- Very expensive

- No proven benefit

- ? harmful


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ColloidsGELA

TINS

DEXTRA

NS

HES

Molecular

weight

28-35

kda

40-70

kda

70-450

kda

Advantages Improves

circulat

ion

Improvescirculatio

n

Improvescirculation,

endothelial

function

Anaphylaxsi

s

High small minimal

VOLUME

EFFECT

SHOR

T

MEDIUM LONGTER

M

COAGULA

TION

+/- ++ +


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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

Volume expansion

Rapid resuscitation

Maintain oncotic pressure

Less tissue oedema

Less pulmonary oedema

Disadvantages:

Coagulation problems

Variable electrolytecontent

Variable half-life

Adverse reactions

EXPENSIVE!


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1.Should not be used except fortreatment

of D. insipidus/ chronic SDH

2.Solution of 5% dextrose ishypoosmolar

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

plasma osmolality.!"#$"%&&$


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osmolality approximately that of plasma.

Eg: NS, Plasmalyte, and Normosol R. Hyperchloremic metabolic acidosis may

result with NS

!"#$"%&&$


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Usually Ringers lactate and/or Normal

Saline

- Avoid dextrose fluids

Infusion rate should be to replace urine

output and insensible losses ml. for ml.

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

haematocrit of 25-30%!"#$"%&&$


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Permissible blood loss

EBV x (HIH

d) /H

I

EBV=weight x avg blood volume


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Increases plasma- cerebral parenchymaosmolality gradient

dose -0.5-2.0 gm/kg

large dose enhances cerebral bloodflow and free radicalscavenging

!"#$"%&&$


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Mechanism of action is similar to mannitol

Strengths of HS 3, 5 7.5%

Increases serum Na+ and hypokalemiacauses less diuresis

!"#$"%&&$


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Transfusion of blood in the form of packed cell ifHb< 8

Dilutional clinical coagulopathy when blood lossexceeds more than one blood volume

Fresh frozen plasma to be administered ifprothrombin time> 1.5 time normal

Dose of FFP: 10- 15 ml/ kg ( to obtain 30% ofplasma factor concentration)

Prophylactic administration contraindicated Platelet deficiency occurs if blood loss exceeds >

1.5 times EBV (14)

Transfusion indicated if counts less than 50,000/

cmm or if higher counts with bleeding!"#$"%&&$


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Dual set of problemsHypovolemia

Hyponatremia- CSW and SIADH

Avoid dehydration Cerebral vasospasm by

hypervolemia by CVP of 8- 10

hemodilution by PCV around 30-35

hypertension

Avoid dextrose containing solutions!"#$"%&&$


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Electrolytes

Normal values

Na+ - 130-149meq/l

K+ - 3.5-5meq/l

Cl- 95-110 meq/l

Ca- 8.1-10.4mg%


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Electrolyte Parenteral Equivalent

of RDA

Usual Intake

Sodium 12 meq/kg +

replacement,

but can be as

low as 540meq/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

Factors controlling sodium Reabsorption


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Factors controlling sodium Reabsorption

in Perioperative Period

RAS:- Renin secretion

increases formation ofAngiotensin IIAldosterone Na reabsorption inDistal tubule

Sympathetic nervous system- IncreasedSympathetic activity increases sodium absorption inproximal tubule

ADH- it has little action on sodium excretion.,it

mostly 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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HYPONATREMIAHypovolumic Hypervolumic EuvolumicCCF

NEPHROTIC SYNDROME

RENAL FAILURE

CIRRHOSIS

Extra renal sodium loss

diarrhea

Vomiting

Blood loss

Excessive sweating

Renal sodium loss

CSWS

Diuretics

Osmotic diuresis

Adrenal insufficiency

ketonuria

SIADHCNS

SOL

Trauma

Hemorrhage

Stroke

Inflammatory

disordersdemyelination

DrugsCarbamazepine

Chlorpropramide

Phenothiazines

SRI

TCA

Pulmonaryconditions

Infections

ALI

Neoplasia

THIAZIDE DIURETICS

HYPOTHYROIDISMADRENAL


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Signs & Symptoms of HyponatremiaModerate-

lethargy

Nausea/vomiting

Irritability

HeadacheMuscle weakness/cramps

SevereDrowsiness

Depressed reflexesSeizures

Coma

Death

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Assesment of Pt with Hyponatremia

Clinical-

Skin turgor & mucous membranes

JVP

Orthostatic variation in pulse and B.P

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

QRS widening,ST elevation,T inversion

Bradycardia, Ventricular ectopics also

possible

At values< 110mmol/l cardiac arrest mayoccur.

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

!0.6

3%NS

Correction rate - 0.6-1mmol/l/hr tillNa=125meq/l

Half the deficit can be administered over 1st 8

hrs, rest over 1-3 days

Correct underlying disorder


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Hypertonic saline - symptomatic

Fluid restriction /Normal saline -

asymptomatic patients

Salt replacement

!"#$"%&&$


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Complication of Treatment

Pontine Myelinolysis - quadriparesis ,ataxia,abnormal extraocular movements. can occur with

rapid correction

Renal Failure, Peripheral edema, pulm

edema, heart failure


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SIADH

Diagnostic Criteria of SIADH:-!"##$%&!'( *+,$%%&-$. /001

Serum sodium serum osmolality

Normal thyroid, adrenal, renal function

Absence of peripheral edema ordehydration

Clinical features are same of hyponatremia


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Specific Treatment of SIADH

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

Furosemide

Lithium - blocks 3,5- AMP & inhibits action of ADHon renal tubule

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

-

Cerebral salt wasting


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Cerebral salt wasting

syndrome

Renal loss of sodium due to intracranialdisease, leading to hyponatremia &hypovolemia

Causes: Head injury

Brain tumor

Stroke Intracerebral hemorrhage

Tuberculous meningitis

Craniosynostosis repair

Cerebral salt wasting syndrome (


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Cerebral salt wasting syndrome (

CSWS )

Pathophysiology not fully understood-hypothesis

natriuretic response due to SNS overactivity

and DA release causes urinary sodium loss

release - brain natriuretic peptide, C-type

natriuretic peptide or an oubain like peptide,

by the injured brain

CSWS usually appears in the first week after

brain injury and spontaneously resolves in 2-

4 weeks


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Specific Treatment of CSWS

Fluid & Sodium Resuscitation -0.9%

saline used

acute symptomatic -hyponatremia 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 acuteperiod(4-10days)

Incidence is 29%-43%2 3$+$#$'4 $5Neurolog res2000; 22:151-55, found

A.Com-51%-a/w hyponatremia

MCA-18% - a/w hyponatremia2 67%&.-$ et al -84% with hyponatremia had

symptomatic vasospasm2 ,$!$. '4 $5 8.. .'"%75 /009:;/?9didnt 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-exist85*$.'!' '4 $5 @

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!"#$"%&&$


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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 byD$EE+

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>;A#$C&.$#)5&

Defined as serum Na >145mmol/l

Clinical variables:

1. Body weight

2. Peripheral oedema

3. CVP

4. Serum sodium/ Urine spot sodium

!"#$"%&&$


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Major causes of hypernatremia

CAUSES

Impaired Thirst

Solute (osmotic) diuresis

Excessive water loss Renal

Extrarenal

Combined disorders

MECHANISMS

Coma,

Essential Hypernatremia

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

Weakness

Neuromuscular irritability

Focal neurological deficit Occasional coma/seizures

Algorithim for assessment of Hypernatremia


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Algorithim for assessment of Hypernatremia

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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

correction should be done

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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!"#$"%&&$

DIABETUS INSIPIDUS


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Central DI

Nephrogenic DI

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1/3rd in SAH and TBI1/6th in pituitary surgery and intracerebral

hemorrhage

CENTRAL DI:-It is a failure of release of ADH from


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It is a failure of release of ADH fromHypothalamo-pituitary axis

Characterised by inability to concentrateurine ,thus passage of large amount ofdilute urine

Rise in Plasma osmolality & progressive

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

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60/92

Etiology of Central DI

Acquired Head trauma

Post-pituitary surgery

Neoplasms Granulomas

Infections

Inflammations

Chemical toxins Tetrodoxins,Snake

venoms

Vascular

Idiopathic

Congenital Midline craniofacial

anomalies

Holoprosencephaly Ectopia of Pituitary

Genetic Autosomal dominant

Autosomal Recessive X-linked recessive

Deletionchromosome7q


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ETIOLOGY OF NEPHROGENIC DI

Vascular SCD

ATN

Granulomas

Neoplasm Infiltrations

Pregnancy

Idiopathic

GeneticX-linked recessive(ADH

receptorV2).

Autosomal Recessive(Aquaporin-2 gene)

Acquired

Drugs Lithium

Demeclocycline

Methoxyflurane Amphotericin B

Aminoglycoside

Cisplatin

Rifampicin

Foscarnet Metabolic

Hypercalcemia

Hypokalemia

Obstruction


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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


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64/92

ALGORITHM FOR DIAGNOSIS OF DI

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65/92

Treatment of postoperative

diabetes insipidusExpectant monitoring

I/O CHARTING

Urine osmolality or specific gravity every 4 to 6 hours,

Serum [Na+] every 4 to 6 hours

Antidiuretic hormone therapy

Desmopressin 1 mg to 2 mg iv/sc10mcg-20mcg nasal

Redose - urine output 200 mL to 250 mL/hr for 2 hours

with urine specific gravity < 1.005

urine osmolality < 200 mOsm/kg H2O

Maintenance


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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 insufficiency

stress 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

Onset slow, efficacy less,efficacy 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 drug

generally cures the disease

Thiazide Amiloride (esp in pts. On lithium)

Indomethacin

Low sodium diet

FLUID DEPRIVATION TEST


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FLUID DEPRIVATION TEST

Indication

Evaluation of Diabetes Insipidus

Precautions: Requires closemonitoring

Monitor urine output

Monitor vital signs

Monitor weight Do not allow weight loss to exceed

>3-5%

CONTD..

TechniqueFl id restrict patient


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

Follow Serum Osmolality to steady state

Serum Osmolality should approach 295 mOsmwater

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

CONTD


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CONTD..

Interpretation Water deprivation effect on urine

concentrating ability

No response in Nephrogenic DI

No response in Central DI

Exogenous ADH effect on urineconcentrating ability

Corrects Central DI Does not correct Nephrogenic DI


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Hypokalemia


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Hypokalemia

Normal requirement 1meq/kg/day

Serum potassium < 3.5 mEq/ liter

Causes: intracellular shift

potassium depletion

6/19/2009

Hypokalemia


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Hypokalemia

Transcellular shift:beta agonists

diuretics

alkalosis

hypothermia

insulin !"#$%%&'()*+,*#&"-./*-$,,"%%*%.)&'/*%&%01$&,'/*

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Clinical features hypokalemia


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Clinical features hypokalemia

Muscle weakness and mental status

changes< 2.5 mEq/ liter ECG changes prominent U waves,

flattening and inversion of T waves,

prolonged QT interval Does not cause arrhythmias on its own

but definitely is proarrythmic

6/19/2009

Hypokalemia


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6/19/2009

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Management of hypokalemia


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Management of hypokalemia

Correct the primary causePotassium deficits in hypokalemia for 70

Kg malef4AEN S8?5CC


78/92

Iv replacement

Potassium chloride- concentration varies from 1 and2 meq/ ml.

Extremely hyperosmololar and must be diluted

Infusion rate: add 20 meq to 100 ml isotonic saline

- rates of 20 mEq/ hour- can go as high as 40 mEq/ hour

- use central line with cardiac

monitoring

-If refractory check for magnesiumdeficiency as it promotes urinary lossesMild cases :Oral potassium chloride (1 TSF=20meq/l ),

2tsf TDS diluted in liquids

6/19/2009


79/92

Serum potassium > 5.5 mEq/ liter Most common cause is traumatic

hemolysis during venipuncture

20% blood sample incidence withelevated potassium

Source: transcellular shift ( urinary

K>30)

renal cause ( urinary K< 30)

!"#$"%&&$


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81/92

Slowing of electrical conduction of theheart

Usually starts when K level reaches 6.0

mEq/ L Tall tented T waves

Decrease in P wave amplitude

PR lengthening

QRS prolongation with eventual

asystole!"#$"%&&$

Management


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g

Guided by serum potassium and ECG

manifestation

1.Severe cases -Give 10 ml- 10% calciumgluconate over 5 minutes

Repeat second dose if necessary

No role for third doseAction lasts for 20 minutes

6/19/2009


83/92

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

6/19/2009

Metabolic acidosis


84/92

High Anion Gap

Renal failure

toxins

ketoacidosis

Normal anion gap (hyperchloremic)

Hyperkalemia

obstructive uropathy diarrhea

renal tubular acidosis

Some medications6/19/2009

Clinical features Headache


85/92

Headache

Drowsiness Nausea/ vomiting/ diarrhea

Kussmauls respirations

Fruity-smelling breathe Hyperkalemia

Hypotension

Bradycardia GI distention

pH low (< 7.35)

HCO3 low (< 22)6/19/2009

Management:


86/92

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 7 206/19/2009


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Metabolic alkalosis


88/92

Clinical features Shallow breathing

Nausea/vomiting/diarrhea

Confusion Numbness / tingling

Hypocalcemia

Hypokalemia

pH high (> 7.45)

HCO3 high (>26) cal features:6/19/2009


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Metabolic alkalosis


90/92

Management: saline infusion (0.2*body

weight* chloride deficit)

In resistant cases give 0.1N HCl (0.5*

body weight* base excess)

Acetazolamide

6/19/2009

Respiratory acidosis and alkalosis


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Treatment of underlying cause

Correction of oxygenation

Sedation, reassurance and CO2

rebreathing for alkalosis

Ventilatory support and chest

physiotherapy

6/19/2009


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fluid and electrolyte balance in neurosurgery.pdf

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