Download Fluids and Electrolytes

Fluid and Electrolyte
Management of the
Surgical Patient
Dr Abdollahi
Afshar Hospital
Fluid therapy is often poorly
taught, poorly understood and
poorly done
‘Fluid therapy should be directed not only to
effective volume expansion of a leaky
circulation but also to micro vascular
protection’.
Fluid and electrolyte management are paramount to
the care of the surgical patient. Changes in both
fluid volume and electrolyte composition occur
preoperatively, intraoperatively, and post
operatively, as well as in response to trauma and
sepsis.
Total Body Water
Who is having higher proportion of body weight as
water? And Why?
􀁻Males or Females
􀁻Lean or Obese
􀁻Young or elderly
Body Fluid Compartments:
2/3
X 50~70%
lean body weight
ICF:
55%~75%
TBW
3/4
•
•
•
•
•
Male (55%) > female (45%)
Most concentrated in skeletal muscle
TBW=0.6xBW
ICF=0.4xBW
ECF=0.2xBW
1/3
ECF
1/4
Extravascular
Interstitial
fluid
Intravascular
plasma
Total body water (TBW)
• TBW varies with age ,gender and body habitus
• In adult males= 55% of body weight
• In adult female=45% of body weight
• In infant = 80% of body weight
• Obese patients have less TBW per Kg than lean body
adult.
Body compartment fluid
1= Intracellular fluid (ICF)=55% TBW or 30%-40% BW
2= Extracellular fluid (ECF) =45%TBW or 20% BW
 Interstitial fluid =15% of body weight
 Intravascular fluid or plasma volume
= 5% of body weight.
Example: men with 70kg
 TBW= 55%70 =38.5 L
 ICF = 55% 38.5 =21.2L
 ECF = 45% 38.5=17.3L
1. ISF = 15%  70 = 10.5L
2. PV = 5%  70 =3.5L
Fluid compartments
ICF
Fluid compartments
ICF
Interstitial
ECF
Fluid compartments
ICF
Interstitial
ECF
Fluid compartments
Capillary
Membrane
ICF
Interstitial
ECF
Fluid compartments
Capillary
Membrane
ICF
Interstitial
ECF
Fluid compartments
Capillary
Membrane
Cell Membrane
ICF
Interstitial
ECF
Colloid osmotic pressure
Capillary
Membrane
Interstitial
ECF
Capillary membrane freely
permeable to water and
electrolytes but not to large
molecules such as proteins
(albumin).
Colloid osmotic pressure
Capillary
Membrane
Interstitial
ECF
Capillary membrane freely
permeable to water and
electrolytes but not to large
molecules such as proteins
(albumin).
Colloid osmotic pressure
Capillary
Membrane
H2O
Interstitial
H2O
ECF
Capillary membrane freely
permeable to water and
electrolytes but not to large
molecules such as proteins
(albumin).
The albumin on the plasma side
gives rise to a colloid osmotic
pressure gradient favouring
movement of water into the plasma
Colloid osmotic pressure
Capillary
Membrane
H2O
H2O
Interstitial
H2O
120/80
H2O
Capillary membrane freely
permeable to water and
electrolytes but not to large
molecules such as proteins
(albumin).
The albumin on the plasma side
gives rise to a colloid osmotic
pressure gradient favouring
movement of water into the plasma
This is balanced out by the
hydrostatic pressure difference
ECF
Cell Membrane
Cell Membrane
H2O
H2O
ICF
Interstitial
Cell membrane is freely permeable to H20 but
Cell Membrane
Cell Membrane
H2O
H2O
Interstitial
ICF
Na+
K+
Cell membrane is freely permeable to H20 but Na and K are
pumped across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane
H2O
H2O
Interstitial
ICF
Na-
K+
[K+] =4
Cell membrane is freely permeable to H20 but Na and K are
pumped across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane
H2O
H2O
Interstitial
ICF
Na-
K+
[K+] =4
[K+] =150
Cell membrane is freely permeable to H20 but Na and K are
pumped across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane
H2O
Na+= 144
H2O
Interstitial
ICF
Na-
K+
[K+] =4
[K+] =150
Cell membrane is freely permeable to H20 but Na and K are
pumped across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane
H2O
Na+=
Na+= 10
144
H2O
Interstitial
ICF
Na-
K+
[K+] =4
[K+] =150
Cell membrane is freely permeable to H20 but Na and K are
pumped across this membrane to maintain a gradient!
Composition of Fluid Compartments
200 mEq/L
154 mEq/L
CATIONS
Na+
142
154 mEq/L
ANIONS
Cl
HC03
-
K+
Ca++
Mg++
Na+
ANIONS
Cl
-
CATIONS
K+
HC03-
3
114
504
4
organic
Acid
5
PLASMA
150
—
30
HCO3-
K+
3 Protein 16
ANIONS
150 HPO4
---
4
5
144
153 mEq/L
27
504—
PO4
CATIONS
103
-
153 mEq/L
200 mEq/L
504—
PO4---
3
organic
Acid
5
Ca++
3
Mg++
2 Protein
INTERSTITAL
FLID
10
1
Mg++
40 Protein
Na+
10
INTRACELLULAR
FLID
40
Composition of Body Fluids:
Cations
150
Anions
100
50
0
ECF
Na+
ClHCO3-
2+
Ca
Mg 2+
Protein
K+
Organic
anion
ICF
50
PO43-
100
150
Osmolarity = solute/(solute+solvent)
Osmolality = solute/solvent (290~310mOsm/L)
Tonicity = effective osmolality
Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)
Plasma tonicity = 2 x (Na) + (Glucose/18)
‫عوامل موثر روی تغییرات آب والکترولیت‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫نوع عمل جراحی (میزان خونریزی‪ -‬تبخیر آب – حجم‬
‫فضای سوم )‬
‫وضعیت آب والکترولیت قبل از عمل‬
‫بیماریهای همراه (اندوکرینوپاتی(‬
‫اثر داروهای بیهوشی (نسدونال‪ -‬پروپوفل‪)RA -MR -‬‬
Reasons for fluid therapy
Preserve oxygen delivery to tissues
•
Correct hypovolaemia
Colloids + RBCs
• Maintain cardiac output
• Optimise gas exchange
• Replace electrolytes & water
Crystalloids
• Maintain urine output
Identify what is the goal
Choose fluid which best achieves the goal
‫ارزیابی حجم مایع داخل عروقی‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫شرح حال بیمار‬
‫فشار خون (ایستاده – خوابیده )‬
‫ضربان قلب بیمار‬
‫برون ده ادراری‬
‫هماتوکریت‬
‫نیتروژن خون‬
‫الکترولیت ها‬
‫‪ABG‬‬
‫‪CVP‬‬
‫محلولهای وریدی‬
Fluids
• Crystalloids
• Colloids
• blood
Which of the following solutions is isotonic?
A. D5W
B. 0.45% saline
C. 0.9% saline
D. D5 in 0.9% saline
Common parenteral fluid therapy
Solutions
Volumes
Na+
K+
Ca2+
Mg2+
Cl-
HCO3-
Dextrose
mOsm/L
ECF
142
4
5
103
27
280-310
Lactated
Ringer’s
130
4
3
109
28
273
0.9% NaCl
154
154
308
0.45% NaCl
77
77
154
D5/0.45%
NaCl
77
77
3% NaCl
513
513
1026
500
154
154
310
250,500
130160
<2.5
130160
330
20,50,100
130160
<2.5
130160
330
D5W
6%
Hetastarch
5% Albumin
25%
Albumin
50
406
Crystalloids:
Isotonic crystalloids
- Lactated Ringer’s, 0.9% NaCl
- only 25% remain intravascularly
• Hypertonic saline solutions
- 3% NaCl
• Hypotonic solutions
- D5W, 0.45% NaCl
- less than 10% remain intravascularly, inadequate for fluid
resuscitation
•
Colloid Solutions:
• Contain high molecular weight
substancesdo not readily migrate across
capillary walls
• Preparations
- Albumin: 5%, 25%
- Dextran
- Gelifundol
- Haes-steril 10%
‫رینگر الکتات‬
‫• مایع نمکی ایزوتونیک جهت جایگزینی از دست دادنهای ‪ GI‬و‬
‫کاهش ‪ ECF‬بدون اشکاالت عمده در ترکیبات و اجزا رینگر‬
‫الکتات است‪.‬‬
‫• ایزوتونیک‬
‫‪Na=130meq/l‬‬
‫• ‪CL=109meq/l lactat=28meq/l‬‬
‫‪osm=273‬‬
‫‪0.9%Nacl‬‬
‫‪• Na=154‬‬
‫‪• CL= 154‬‬
‫• این مایع جهت جبران کاهش ‪ ECF‬در حضور هیپوناترمی‬
‫وهیپوکلرمی و آلکالوز متابولیک ایده ال است‪PH=5.6.‬‬
Postoperative (maintenance)
0.45%Nacl +5% dextrose +KCL
Perioperative management of fluid balance
include:
1. Preoperative evaluation
2. Intraoperative maintenance
3. Replacement of fluid losses
Preexisting fluid deficits
• NPO time and abnormal fluid losses (vomitingdirreha- asites- infected tissue-fever –sweatinghyperventilation)
• Hypotonic fluid (0.5% saline ) or isotonic
crystalloids
Maintenance requirements
• Up to 10 kg
= 4cc/kg/hr
• 11-20kg
= add 2cc/kg/hr
• 21kg and above = add 1cc/kg/hr
• Insensible losses = 2cc/kg/hr
Surgical fluid losses
Blood loss (measurement)
1. Suction container
2. Surgical sponge
3. Hct and tachycardia not specific
4. ABG and UO if hypoperfusion occur
5. Blood loss=3/1 with crystalloid
Other losses (third space loss)
Third space loss
1. Minimal (herniorrapy) =2-4cc/kg/hr
2. Moderate (cholecystectomy)=4-6cc/kg/hr
3. Severe (bowel resection) = 6-8cc/kg/hr
Crystalloid solution
1.
2.
3.
4.
The main solutions is either glucose or saline
Hypotonic or isotonic or hypertonic.
Safe , nontoxic, reaction free ,inexpensive.
Complication is edema if large volumes are
needed.
5. During surgery isotonic solution favored
(normal saline - lactate ringer and plasma lyte)
Colloids
1. Albumin
2. Hydroxyethyl starch
3. Dextran
Complications
1.
2.
3.
•
•
Hypersensitivity reactions (anaphylaxis )
Pruritis (hetastarch)
Couglopathy (dextran 70 and hetastarch) > 1 litter
Dextran ( platelet aggregation , adhesive)
Hetastarch (reduction in factor vlll and VOB factor
)
These colloid is best avoided in patients with
coagulopaty.
The Influence of Colloid & Crystalloid on
Blood Volume:
Blood volume
Infusion
volume
200
1000cc
500cc
500cc
500cc
600
1000
Lactated Ringers
5% Albumin
6% Hetastarch
Whole blood
Colloid versus crystalloid solutions
Transfusion consideration
• HB <7 mg /dl increase CO
• Ideal Hb is 7-8 mg/dl
• In IHD patients or pulmonary disease > 10
mg/dl
‫اختالل در حجم مایعات بدن‬
1. Fluid volume deficit
2. Fluid volume excess
‫‪Fluid volume deficit‬‬
‫)‪(FVD‬‬
‫کاهش آب والکترولیتهای بدن( به نسبتی که در مایعات طبیعی بدن‬
‫وجود دارد ) به صورتی که نسبت الکترولیتهای بدن به آب‬
‫یکنواخت باقی بماند کاهش حجم مایع ‪ FVD‬به وجود خواهد‬
‫آمد (کاهش ایزوتونیک)‪.‬‬
‫میزان الکترولیتهای سرم در‪ FVD‬نرمال باقی میماند مگر اختالل‬
‫دیگری همراه با آن باشد‬
‫‪DEHYDRATION‬‬
‫• در دهیدریشن کاهش آب همراه با افزایش سدیم سرمی وجود‬
‫دارد‪.‬‬
‫علل کاهش حجم خارج سلولی‬
‫‪ .1‬از دست دادن غیر طبیعی آب بدن‪:‬استفراغ –اسهال‪- -‬تعریق‪-‬‬
‫‪NGT‬‬
‫‪ .2‬کاهش میزان دریافت آب بدن‪:‬تهوع یا ناتوانی دسترسی به‬
‫مایعات‬
‫‪ .3‬خروج مایعات از سیستم کاردیواسکوالر ( ‪third space‬‬
‫‪ )loss‬مثل سوختگی –ترومای جراحی‬
Signs of Hypovolemia:
• Diminished skin turgor
• Dry oral mucus membrane
• Oliguria
- <500ml/day
- normal: 0.5~1ml/kg/h
• Tachycardia
• Hypotension
• Hypoperfusioncyanosis
• Altered mental status
Clinical Diagnosis of Hypovolemia:
• Thorough history taking: poor intake, GI
bleeding…etc
• BUN : Creatinine > 20 : 1
- BUN↑: hyperalimentation, glucocorticoid
therapy, UGI bleeding
• Increased specific gravity
• Increased hematocrit
• Electrolytes imbalance
• Acid-base disorder
Signs of Hypervolemia:
•
•
•
•
•
Hypertension
Polyuria
Peripheral edema
Especially when hypoalbuminemia
Wet lung
Jugular vein engorgement
Management of Hypervolemia:
• Prevention is the best way
• Guide fluid therapy with CVP level or
pulmonary wedge pressure
• Diuretics
• Increase oncotic pressure: FFP or
albumin infusion (may followed by diuretics)
• Dialysis
Fluid Management:
• Goal:
- to maintain urine output of
0.5~1.0mg/kg/h
• Rule:
• Electrolytes require:
- Na+: 1-2mmol/kg/day
- K+: 0.5~1.0mmol/kg/day
• Avoid fluid overload, especially in malnutrition,
heart failure and renal insufficiency patient
Electrolyte physiology
Sodium physiology
 Na
is the most abundant positive ion of ECF
compartment and is critical in determining the
ECF and ICF osmolality.
 Normal amount 135-145 meq/l
Osmotic Pressure
Calculated serum osmolality =
2 sodium+ glucose/18 + BUN /2.8
Osmolality = 290 mosm
Concentration
1.Serum sodium concentration
2.Serum osmolarity
• Hypovolemic/hypernatremic (burn, fever)
• Hypovolemic/hyponatremic (vomiting ,diarrhea or fistula
drainage)
• Normovolemic/hyponatremic (decrease kidney reserve )
• Hypervolemic/hyponatremic (excessive water intake,TURP,
DW5%)
Hypernatremia
Serum Na>145mEq/L
Hypernatremia:
Loss of Free Water
- Hypernatremia
Gain of sodium in excess of water
Hypo volemic
-Hypernatremia
Hyper volemic
Normo volemic
Hypernatremia

Volume Status

High
Normal
Low
Iatrogenic sodium
administration
Nonrenal water loss
Nonrenal water loss
Skin
Mineralocorticoid excess
Aldosteronism
Cushing’s disease
Congenital adrenal
hyperplasia
Skin
Gastrointestinal losses
Gastrointestinal
Renal water losses
Renal water loss
Renal (tubular) Diuretics
Renal disease
Diuretics
Diabetes insipidus
Osmotic diuretics
Diabetes insipidus
Adrenal failure
Asymptomatic
Hypernatremia
Symptomatic (Na>160 meq/L)
Clinical Manifestations of Abnormalities in Serum Sodium
Body system
Central nervous system
Musculoskeletal
Cardiovascular
Tissue
Renal
Metabolic
hypernatremia
Restlessness, lethargy, ataxia, irritability, tonic spasms,
delirium, seizures, coma
weakness
Tachycardia, hypotension, syncope
Dry sticky mucous membranes, red swollen tongue,
decreased saliva and tears
Oliguria
Fever
Treatment
Normal saline in hypovolemic patients
Hypotonic fluid (D/w 5%, D/W 5% in ¼ or ½ normal
saline, or entral water)
The formula used to estimate the amount of water
required to correct hypernatremia:
Water deficit (L)=
Serum sodium-140
× TBW
140
Estimate TBW as 55% of lean body mass in men and
45% in women
The rate of fluid administration:
1.
Acute hypernatremia: a decrease in serum sodium
of no more than 1meq/h and 12meq/d
2.
Chronic hypernatremia: a decrease in serum
sodium of no more than 0.7meq/L/h
Hyponatremia:
Na<135mEq/L
Causes :
1. Sodium depletion
2. Sodium dilution
• Incidence = 4.5%
• After surgery=1%
• Mortality = 2 times normal
Sodium depletion
1. Decrease intake
􀁻Low Na diet
􀁻Enteral feeds
2. Increase loss
Gastrointestinal Losses
􀁻Vomiting
􀁻Prolonged NGT suctioning
􀁻Diarrhea
Renal Losses
􀁻Diuretics
􀁻Primary renal disease
3. Depletional hyponatreamia is often accompanied by
extracellulr volume deficit
Sodium dilution
1. Due to excess extracellular water
􀁻Intentional: excessive oral intake
􀁻Iatrogenic: Intravenous
2. Drugs
􀁻Antipsychotics
􀁻Tricyclic antidepressants
􀁻Angiotensin-converting enzyme inhibitors
3. Hyperosmolar
􀁻Mannitol
􀁻Hyperglycemia
4.Pseudohyponatremia
􀁻Plasma lipids
􀁻Plasma proteins
Sign and symptoms
• CNS symptom when Na<123 meq/l
• Cardiac symptom when Na<100 meq/l
For every 100 mg/dL increment in plasma glucose above normal,
the plasma sodium should decrease by 1.6 mEq/L.
Clinical Manifestations of Abnormalities in Serum Sodium
Body System
Hyponatremia
central nervous system
Headache, confusion, hyper-or hypoactive deep tendon
reflexes, seizures, coma, increased intracranial pressure
Weakness, fatigue, muscle cramps/twitching
Anorexia, nausea, vomiting, watery diarrhea
Hypertension and bradycardia if significant increases in
intracranial pressure
Lacrimation, salivation
Oliguria
Musculoskeletal
Gastrointestinal
Cardiovascular
Tissue
Renal
Treatment
1=Depend on ECF
2=CNS sign
Treatment
1. Asymptomatic : increase the sodium level by no more than
0.5-1 meq/L/h to a maximum increase of 12 meq/L per day
2.
Symptomatic: (Na<120 meq/L) Increase the sodium level by no
more than 1meq/L per hour until the serum Na level reaches 130
meq/L or neurologic symptoms are improved
Rapid correction of hyponatremia

Pontine myelinolysis

Seizures, weakness/paresis, akinetic
movements, unresponsiveness

Permanent brain damage

Death
‫‪Dose‬‬
‫‪Na deficit meq =(140- Na meq/l) TBW‬‬
‫اصالح باید‪ 0.5-1 meq/l /h‬باشد تا سدیم به ‪125meq/l‬برسد و‬
‫سپس آهسته اصالح شود ‪.‬‬
Potassium abnormalities
• The average dietary intake of potassium: 50-100meq/d
• The average renal excretion of potassium: 10-700 meq/d
- 2% of the total body potassium in ECF (4.5meq/L)
- Factors that influence serum potassium:
1.
Surgical stress
2.
Injury
3.
Acidosis
4.
Tissue catabolism
Hyperkalemia
The normal range of serum potassium: 3.5-5 meq/L
Etiology of Hyperkalemia
Increased intake
Potassium supplementation
Blood transfusions
Endogenous load/destruction:
hemolysis, rhabdomyolysis,
cruch injury, gastrointestinal hemorrhage
Increased release
Acidosis
Rapid rise of extracellure osmolality (hyperglycemia or mannitol)
Impaired excretion of potassium
Renal insufficiency/failure
Clinical manifestation of hyperkalemia
System
hyperkalemia
Gastrointestinal
Neuromuscular
Cardiovascular
Nausea/vomiting ,colic, diarrhea
weakness, paralysis, respiratory failure
Arrhythmia, arrest
ECG changes
Peaked T waves (early change)
Flattened P wave
Prolonged PR interval (first-degree block)
Widened QRS complex
Sine wave formation
Ventricular fibrillation
Treatment
Treatment of symptomatic hyperkalemia
Potassium removal
Kayexalate
Oral administration is 15-30 g in 50-100 mLof 20% sorbitol
Rectal administration is 50 g in 200 mL 20% sorbitol
Dialysis
Shift potassium
Glucose 1 vial of D50% and regular insulin 5-10 units intravenous
Bicarbonate 1 vial intravenous
Counteract cardiac effects
Calcium gluconate 5-10 mL of 10% solution
Hypokalemia
Etiology :
inadequate intake
Dietary, potassium-free intravenous fluids, potassium-deficient
total parenteral nutrition
Excessive potassium excretion
Hyperaldosteronism
Medications
Gastrointestinal losses
Direct loss of potassium from gastrointestinal fluid (diarrhea)
Renal loss of potassium (gastric fluid, either as vomiting or high
nasogastric output)
Intracellular-shift (metabolic alkalosis or insulin therapy)
Potassium changes associated with
alkalosis:
Potassium decrease by 0.3 meq/L for every 0.1
increase in PH above normal
Magnesium Depletion
(drug induced: amphotericin, amioglycosides, cisplatin)

Renal potassium wastage

Hypokalemia
Clinical Manifestation of Abnormalities in potassium
System
Gastrointestinal
Neuromuscular
Cardiovascular
ECG changes
hypokalemia
Ileus, constipation
Decreased reflexes, fatigue, weakness,
paralysis
Arrest
U-waves
T-wave flattening
ST-segment changes
Arrhythmias
Treatment
Electrolyte Replacement Therapy Protocol
Potassium
Serum potassium level <4.0 mEq/L
Asymptomatic, tolerating enteral nutrition: KC1 40 mEq per entral access
× 1 doses
Asymptomatic, not tolerating entral nutrition: KC1 20 mEq IV q2h × 2 doses
Symptomatic: KC1 20 mEq IV q1h × 4 doses
Recheck potassium level 2 hours after end of infusion; if <3.5 mEq/L and
asymptomatic, replace as per above protocol
•
•
Oral repletion for mild and asymptomatic hypokalemia
IV repletion for severe and symptomatic hypokalemia
‫‪Calcium‬‬
‫•‬
‫•‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫بیش از ‪ %99‬از كلسیم بدن در سیستم اسكلتي است (استخوان‬
‫–دندانها)‪.‬‬
‫نقش كلسیم‪:‬‬
‫انتقال ایمپالسهاي عصبي)‪(NMJ‬‬
‫انقباض عضالت صاف‬
‫مسبب آزادسازي آنزیمهاي الزم برای واكنش هاي شیمیائي‬
‫انعقاد‬
‫‪ Ca<4.5 meq/l‬هیپوكلسمي یونیزه‬
‫•‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫‪.5‬‬
‫‪.6‬‬
‫‪.7‬‬
‫علل‪:‬‬
‫كم كاري پاراتیروئید‬
‫پانكراتیت‬
‫نارسائي كلیه (احتباس فسفر و مختل شدن تبدیل ویتامین ‪ D‬به فرم فعالش در کلیه)‬
‫هیپرونتیالسیون (آلكالوز تنفسي) باعث افزایش باند شدن کلسیم با آلبومین میشود‪.‬‬
‫ترانسفیوزن ماسیو‬
‫تخلیه منیزیوم (مهار ترشح پاراتورمون)‬
‫انفوزیون بیکربنات (کلسیم به طور مستقبم با بیکربنات تزریق شده پیوند می شود)‪.‬‬
‫عالئم هیپوکلسمی‬
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‫هیپر رفلکسی‬
‫تشنج‬
‫تتانی‬
‫‪ 25%( Chevostek‬افراد نرمال وجود دارد)‬
‫‪(Trousseau‬در ‪ 30%‬موارد هیپوکلسمی وجود ندارد)‬
‫هیپوتانسیون‬
‫کاهش برون ده قلبی‬
‫آریتمی‬
‫سایرعالئم‬
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‫كاهش قدرت انقباضي قلب‬
‫افزایش فشار ورید هاي مركزي‬
‫كاهش فشار خون‬
‫اسپاسم حنجره‬
‫اسپاسم عضالت اسكلتي‬
‫درمان‬
‫• بر طرف کردن علت زمینه ای‬
‫• کلسیم وریدی‬
‫‪ Ca>5.5meq/l‬هیپركلسمي‬
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‫هیپرپاراتیروئیدیسم‬
‫كانسرها با متاستاز استخواني‬
‫بی حرکتی طوالنی مدت‬
‫داروها (لیتیوم – دیورتیک )‬
‫عالئم‬
GI
Cardiovascular
Renal (polyuria)
CNS
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‫عالئم قلبی‬
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‫اختالالت هدایت قلبي (افزایش فاصله ‪ P-R‬پهن شدن ‪QRS‬وكوتاه‬
‫شدن ‪)Q-T‬‬
‫‪Ca>7 meq/l‬‬
‫درمان‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫‪.5‬‬
‫انفوزیون محلول نمکی ایزوتونیک‬
‫الزیکس‬
‫کلسی تونین‬
‫کورتون‬
‫دیالیز‬
Magnesium Abnormalities
Normal dietary intake: 20meq (240mg)
Excretion in both the feces and urine
Normal serum level: 1.9-2.5 mg/dL
‫منیزیوم‬
‫• دومین کاتیون فراوان داخل سلولی است‪.‬‬
‫• نقش آن به عنوان فاکتور کمکی در واکنش های آنزیمی و در‬
‫حفظ قدرت انقباضی قلب و تون عروق محیطی دارد‪.‬‬
‫• ‪ 55%‬به شکل یونیزه (فعال) و‪ 45%‬باند پروتئین است‪.‬‬
Hypermagnesemia
Etiology:
1.
Impaired renal function
2.
Excess intake (in the from of TPN or magnesiumcontaining laxatives and antacids)
Clinical manifestation hypermanesemia
System
Gastrointestinal
Neuromuscular
hypermanesemia
Nausea/vomiting
Cardiovascular
weakness, lethargy, Decreased
reflexes
Hypotension, arrest
ECG changes
Increased PR interval
Widened QRS complex
Elevated T waves
Treatment
1.
2.
3.
4.
Withhold exogenous sources of magnesium
Correct volume deficit
Correct acidosis if present
Calcium chloride (5-10 ml) to manage acute symptoms
(cardiovascular effects)
5. Dialysis (if elevated levels or symptoms persist)
‫عالئم‬
• Patellar reflexes lost:
• Respiratory depression:
• Respiratory paralysis:
• Cardiac arrest:
8-10 meq/L
10-15 meq/L
12-15 meq/L
25-30 meq/L
Hypomagnesemia
Calcium/ magnesium receptors on renal tubular cells is primarily responsible for mg
homeostasis.
Etiology:
1. Poor intake (starvation, alcoholism prolonged use of IV fluids, and TPN with
inadequate supplementation of magnesium)
2. Increased renal excretion (alcohol, most diuretics, and amphotericin B)
3. GI losses (diarrhea)
4. Malabsorption
5. Acute pancreatitis
6. Diabetic ketoacidosis
7. Primary aldosteronism
Clinical manifestation of hypomagnesemia:
(similar to hypocalcemia)
1. Hyper active reflexes, muscle tremors, tetany with
chevostek’s sign
2. Delirium and seizures in severe deficiency
3. ECG changes:
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Prolonged QT and PR interval
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ST-segment depression
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Flattening or inversion of P waves
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Torsades de pointes
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Arrhythmia
Treatment
1. For asymptomatic and mild hypomagnesemia administer oral
mg.
2. For severe deficit (<1meq/L) or symptomatic patient
administer 1 to 2 g of mg-sulfate IV over 2 minute
(simultaneous with ca-gluconate).
Message for Today
• Do not reccussitate sick patients with any
Dextrose solution.
5% Dex
ICF
Interstitial