Part 07. Pathophysiology of body fluid

PART Ⅶ. Pathophysiology of body fluid and fluid therapy

Part . Pathophysiology Of Body Fluid And Fluid Therapy

Chapter 46. Water

Total Body Water    

; *78% of body weight at birth

; *55-60% of body weight at 1year(adult level)

    - adult female(55%) , adult male(60%) ; due to body fat  

; *TBW(L) = 0.61×wt(Kg) + 0.251

Fluid Compartment

; fetus

    - *ECF>ICF --> 1 세경에 adult level 도달    

    - normal old child (adult level)

           / *ECF(20-25%) : plasma5%+interstitial water 15%+transcellular water 1-3%

     / ICF(30-40%)

     / transcellular fluid(2%)

     / slowly exchangeable compartment(8-10%) : bone, connective tissue, cartilage

# ※객Transcellular Fluid

 1. *GI secretion ; important

 2. urine in the kidney & lower urinary tract

 3. CSF

 4. intraocular

 5. pleural fluid

 6. peritoneal fluid

 7. synovial fluid

Regulation Of Body Water

; plasma osmolarity

    - 285-295mOsm/KgH2O

-body내의 water amount feedback system(involving  

 +--1.osmoreceptor & voilume receptor

 |  2.hypothalamus

 |  3.post.pituitary

 +--4.collecting duct of nephron)

      의해 조절된다.

Inatke

; stimulated by a sensation of thirst

    - *thirst center : mid-hypothalamus

; osmolarity change

    - monitored by

           1. osmoreceptor in hypothalamus, pancreas, hepatic portal vein

         2. baroreceptor in atria, vascular bed

           3. renin-angiotensin system

; *Disorders Of Thirst Mechanism

    1. psycologic disorders

    2. CNS disease

  3. potassium deficiency                     

  4. malnutrition                            

    5. alteration in the RAS system

    --> lead to incresed drinking

Excretion

# Obligatory Loss Of Water

  ; insensible water loss - evaporation from lung and skin

    ; urinary excretion - urine volume to excrete solute load

    ; stool water losses

# urine volume and concentration regulation

   1.ADH;(neurohypophyseal-renal axis)

   2.diet

   3.GFR

   4.state of  renal  tubular epithelium

   5.plasma concentration of adrenal steroids

# urinary water excretion : 2 complementary mechanism 의해 조절

   1.production, storage and release into the circulation of ADH

   2.renal epithelial tubular cell response to ADH

# ADH

  ; supraoptic nuclei에서 생산

  ; secretion;regulated by effective osmotic pressure of the extracellualr fluid

  ; primary action

           - increse the permeability of renal collecting ducts to water

    ; threshold for release of ADH

           - *280mOsm/KgH2O

Pathophysiologic Conditions

# Diabetes insipidus

  ; central : supraoptic-osmoreceptor-hypophyseal axis이상으로 ADH분비(-)

    ; nephrogenic : ADH 정상분비되나 renal collecting duct ADH receptor 이상

Factors Altering ADH Release

# stimulant factors

    ; stressful stimuli - trauma, burn, surgery

    ; nicotine, prostaglandine, cholinergic & beta adrenergic drugs  

    ; demerol, morphine, barbiturate

# inhibitory factors

    ; alcohol - potent inhibitor

    ; dephenyhydantoin(dilantin)

  ; glucocorticoids

Factors Altering The Renal Response To ADH

ADH작용  ;+- unabsorbable,osmotically active solutes in renal tubular

             |  lumen   e.g)glucose in diabetesllitus

             +- intrinsic renal condition

                e.g)tubular damage due to urinary tract obstruction,

Mechanisms For Distributing Fluid Within The Body

 1)ICF volume is maintained by osmotic forces operating across cell membranes

Maintenance Of The ECF Volume

    ; oncotic pressure

           - colloid osmotic pressure

           - exerted by molecules, *primarily albumin

           - produce effective osmotic gradient across capillary walls

 2)plasma volume(plasma water)is maintained by a balance between filteration and

  oncotic forces at the capillary level

 3)interstitial fluid volume may increased by an increse in the hydroststic pressure

 4)transcellularfluid 

  +- inflammatory bowel d's

  +- early severe diarrhea

  +- ileus with multiple fluid level

Osmolality Of Body Fluid

 1) plasma osmorlarity증가(e.g. hyperglycemia,hyperlipidemia):ICF에서 ECF

     water shift, plasma sodium level 감소

 2) pseudohyponatremia ; Tx 필요없다.

Chapter 47. Sodium

Body Content And Distribution Of Sodium

   -58mEq/Kg; 이중 30% non exchangeable or only slowly exchandeable

   -25mEq/Kg; 43.1% bone 존재

   -exchangeable sodium content

    +--fetus;85mEq/Kg

    +--adult;40mEq/Kg

   -Distribution of body sodium

    +-ICF;10mEq/Kg

    +-ECF;140mEq/Kg

    Na-K ATPase and Mg activatedATPase system 의해cell로부터 Na active

        extrusion 이루어진다.

    ATPase inhibitor   1.Ca

                       2.ouabain(digitalis 비슷한 작용을 나타내는 강심제)

                       3.cardiac glycoside

    "sick cell syndrom";total body sodium change없이 ICF ECF사이에 sodium

                          redistribution observed in the serevely  ill patient

Regulation Of Sodium

Intake

Absorption

; throughout GI tract

    - *maximally in jejunum, minimally in stomach

; *by Na-K activated ATPase system

; augmented by aldosterone or DCA(desoxy corticosterone acetate)

Excretion

    concentration of sodium in sweat;5-40 mEq/Kg

  +-  ;cystic fibrosis,addison d's

  +-  ;sodium depletion,hyperaldosteronism

Renal Regulation Of Sodium Excretion

Glomerular Filtration Of Sodium

    +-ECF vol.감소 sodium reabsorption

    +-ECF vol.증가 ANP(atrial natriuretic peptide)분비→ GFR증가→ urine Na증가

Tubular Reabsorption Of Sodium

Fig. 47-2

    +-filtered Na;2/3 is reabsorbed by proximal convoluted tubule;

    |            by avtive transport

    +-Henle's loop(ascending limb);secondary toactive teansport of chloride;

    |           by countercurrent multiplier system

    +-distal convoluted tubule & collecting tubule;fine regulation;by aldosterone

           this is governed by the renin-angiotensin system

                                   potassium balance

                                   trophic hormone

Factors Regulating Sodium Excretion

Renin-Angiotension System

Aldosterone

    ; secretion by angiotensin II

    ; *promoter of sodium reabsorption in late distal convoluted tubule and collecting duct

    ; increase potassium secretion

Atrial Natriuretic Peptide(ANP)

 ; sodium & water excretion증가

 3) starling forces : rapid expansion of ECF vol. interstitial hydrostatic pr.증가

    sodium reabsorption방해, urinary sodium excretion증가

Pathophysiologic Conditions

Hypernatremia

    - serum Na 150meq/L 이상

Table 47-1

Hyponatremia

    ; serum Na 130 meq/L 이하

    ; *common cause

           - decreased nutritional sodium intake due to WIC syndrome

Table 47-2

Chapter 48. Potassium

Body Content And Distribution Of Potassium

    in adult : 53 mEq/kg body weight (95% exchangeable)

   +--intracellular potassium amount : 48 mEq/kg (89.6%)

   +--extracellular potassium amount : 5.5 mEq/kg ( 이중 4mEq/kg bone 존재)

   +--intracellular concentration of potassium : 150 mEq/L

   +--extracellular concentration of potassium : 4-5 mEq/L 

Regulation Of Potassium

# Two Mechanism

    1) extrarenal mechanism

    2) renal mechanism

1) Acute Loads

# absorption

    ; upper GI tract 에서 complete           

    ; lower bowel lumen내에서 sodium exchange

# excretion

    ; renal excretion

           - first 4-6hr one half

    ; extrarenal excretion

           - *translocated into cell, primarily in the liver & muscle

           - *more than 40%

           - regulated by insulin, epinephrine enhancing potassium uptake

                   / mediated through β-receptors

           - aldosterone

                   / increase transport of potassium to muscle

                   / *primary extrarenal site : GI tract

    ; acid-base balance

           - *every 0.1 unit change in blood pH --> change 0.3-1.3mEq/L in opposite direction

2) Chronic Loads

    ; *primarily regulation by kidneys

    ; proximal convoluted tubule 에서 filtered potassium 60% 이상이 재흡수된다      

    ; Factors affecting distal nephron potassium secretion

    mineralocorticoid activity

    dietary potassium

    acid-base status

    distal tubular flow rate

    sodium delivery to distal tubule

  ; aldosterone

           - major role in potassium regulation

        - distal tubule에서 luminal membrane permeability 변경시켜 luminal Na+ cellular K+교환

   * acute potassium load extrarenal protective mechanism

      - 4-6hr내에  1.1/2;kidney통해 배설

                     2.more than 40%;liver muscle내의 cell내로 이동시킴

                     3.some;intestine으로 secretion

      -관여하는 factor

           1.insuline & epinephrine;enhance K+ uptake by liver& muscle

           2.aldosterone;GI tr에서 K+ 배설 증가

           3.glucocorticoid

           4.acid-base balance

              systemic acidosis;movement of K+ out of cell

              systemic alkalosis;opposite effect

              pH 0.1 unit change 0.3-1.3mEq/L K+이동

Pathophysiologic Conditions

Hyperkalemia

Consequence Of Hyperkalemia

      -heart 특히 hyperkalemia susceptible

       paresthesia    weakness    flaccid paraysis

        EKG   peaked T wave

                PR interval prolong

                QRS complex widening(later)

                ventricular fibrillation

Causes

    ; renal excretory impairment

           - *often

    acute or chronic renal failure, adrenal insufficiency, hyporeninemic hypoaldosteronism, use of potassium-sparing diuretics

    acute K+ intake

           - potassium salt of penicillin

    acute tissue breakdown

           - trauma, surgery, burn, cell lysis from chemotherapy

    transcellular redistribution of K+

           - metabolic acidosis, shortly before death, severely ill patients

    *succinylcholine, digitalis overdose

# Pseudohyperkalemia

    ; RBC lysis during collection or handling of blood sample or K+ release fron platelet during clotting

Hypokalemia

Consequences Of Hypokalemia

# serum potassium 1 meq/L감소시 body potassium 10-30% 해당

# Functional Alteration In Skeletal Muscles, Smooth Muscles, Heart

    ; cardiac manifestations

           - ECG changes

                   / *observable

                   / prolonged QT interval & flattened T waves

    ; skeletal muscles

           - weakness : early manifestation noted first in limb muscle

           - areflexia, paralysis, death from respiratory muscle failure

    ; smooth muscles

           - paralytic ileus, gastric dilatation

# serious neurologic symptoms

    ; autonomic insufficiency, orthostatic hypotension, tetany, decreased neuromuscular excitability

           - weakness, decreased bowel motility

# *rhabdomyolysis

# In kidney

    ; vacuolar changes in tubular epithelium

           --> *if sustained, nephrosclerosis, interstitial fibrosis

           --> reduced ability to concentrate or dilute

           --> polyuria, polydypsia

           --> increased HCO3 reabsorption, H+ secretion

           --> systemic alkalosis

# Paradoxical aciduria

  ; extrarenal K+ loss

           --> ICF에서 ECF K+ shift

    --> intracellular potassium is replaced by Na+, H+, dibasic aminoacids

           --> *if severe, excessive exchange of intracellular hydrogen of renal tubular cells for sodium in distal tubule fluid

           --> *systemic alkalosis, aciduria, with increased urinary ammonia excretion

Causes       

renal loss

   )diuretics;osmotic diuretics,carboni anhydrase inhibitor

   )tubular defect;renal tubular acidosis

   )acid-base disturbance

   )endocrinopathy;cushing SD

                     primary aldosteronism

                     thyrotoxicosis

   )diabetic ketoacidosis

   )Bartter syndrom

   )Mg deficiency

extrarenal loss

   )from G-I

     diarrhea,chronic catharsis,frequent enema,protracted vomiting,

     biliary drainage,enterocutaneous fistula

   )from skin;profuse sweating

prolonged decrease intake

Chapter 49. Chloride

Body Content And Distribution Of Chloride

  : major anion of ECF ( plasma 13.6%, interstitial lymph 37.3%, connetive t's 17%,

                         bone 15.2%, ICF 12.4%, transcellular 4.5%)

Regulation Of Chloride

: sodium 병행

Pathophysiologic Conditions

Hypochloremia

   +--1.metabolic alkalosis

   |  2.chloride loss in excess of sodium loss : vomiting,chloride diarrhea,gastric

   |    drainage. metabolic acidosis or K+ deficiecncy 교정할 ,urinary chloride

   |    loss Na+ loss exceed한다.

   +--3.pretracted inadequate intake(chloride-deficient milk formula잔기간 먹일때)

      -K+ deficiency K+ deficit correct전에 K+,Cl- 주어야

      -Sx;failure to thrive,muscle weakness,loss of appetite,lethargy

Hyperchloremia

: distal renal acidosis, parenteral aminoacid sol.

Anion Gap

; Na+ - [Cl- + HCO3-]

; normal : 8-16mEq/L (평균;12mEq/L)

; 임상적의의

    - combined concentration of unmeasured anions such as phosphate, sulfate,protein,organic acid

; Normal Anion Gap

    - renal tubular acidosis

    - stool loss of bicarbonates

; Increased Anion Gap

  - renal failure

           / due to increased phosphate & sulfate

  - diabetic ketoacidosis

           / due to β-hydroxybutyrate and acetoacetate

  - lactic acidosis

           / due to lactate

    - hyperglycemic non-ketotic coma

           / due to unidentified organic acids

    - disorders of aminoacid metabolism

           / due to various organic acids

    - aministration of large amount of penicillin

    - ethylene glycol ingestion

           / due to glycolate production

    - methanol ingestion

           / due to formate production

    - salicylate poisoning

           / due to salicylate anions

; Decreased Anion Gap

  - nephrotic syndrome: due to decreased s-albumin

    - lithium ingestion : due to lithium as unmeasured cation

    - multiple-myeloma : due to cationic protein

Chapter 50. Calcium

Body Calcium

    calcium  +-40%;protein bound(이중 80-90% albumin bound)

             +-60%;free ionic calcium(4.8mg/dl)

Regulation Of Calcium

    Regulation 주로 G-I tr통해

    - 흡수;duodenum proximal jejunum에서 1.25(OH)2vitD3 작용에 의해 흡수

           hypocalcemia parathyroid hormone release stimulation하여

           25(OH)2vitD3 conversion시킨다.

Intestinal Tract Absorption Of Calcium

; primary regulation of calcium

# Increased Absorption

    ; low calcium intake

    ; in growing child

    ; pregnancy

    ; depletion of body calcium store

    ; vitamin D or PTH

    ; pathologic condition

           - sarcoidosis, carcinomatosis, multiple myeloma

# Decreased Absorption

    ; *presence of phytate, oxalate, citrate in GI tract

    ; complex dietary calcium

    ; incresed gastric motility

    ; reduction of bowel length

    ; protein depletion

Renal Calcium Excretion

     excretion : glomerulus filtered non-protein-bound calcium 99% tubule 의해                    재흡수 된다.

     resorption  +-proxiaml tubule(50-55%)---+  Na resorption 평행

                 | loop of henle(20-30%)  ---+                   

                 | distal convoluted tubule(10-15%)---+ independent of Na transport

                 +-collecting duct(2-8%)           ---+

     - Ca reabsorption    by 1.25(OH)2vitD3

       Ca reabsorption    by thyrocalcitonin

     - urinary Ca+ excretion 

     1)expansion of ECF volume

     2)osmotic diuretics,furosemide,thiazide,GH,thyroid H.glucagon투여

     3)metabolic acidosis

     4)prolonged fasting

     5)serum phosphate level 

     6)thyrocalcitonin

    - total calcium level serum albumin level 따라 변화한다.

    - hypoalbuminemia serum total albumin level 낮아도 symptom 없을 있다.

      (  serum ionized calcium level 정상이기 때문에)

- pH change

       ionized Ca++ concentration 10%변동

       acidosis Ca++  ,alkalosis Ca++ 

       rapid correction or overcorrection of acidosis

       symptomatic hypocalcemia초래

   - hypernatremia treatment with low potassium content

       hypocalcemia초래

Pathophysiologic Conditions

Symptomatic Hypocalcemiaa(Low Ca++)

# ★원인

  ; vitamin D deficiency

           - by nutrition deficiency, malabsorption, abnormal metabolism of vitamin D

  ; hypoparathyroidism

    ; pseudohypoparathyroidism

    ; hyperphosphatemia

    ; *Mg deficiency

    ; acute pancreatitis

# neonate hypocalcemia

    ; hypoparathyroidism

    ; abnormal vit,D metabolism

    ; low calcium intake

    ; high phosphate intake   

Hypercalcemia

# ★원인

  ; 1' or 3' hyperparathyroidism

  ; hyperthyroidism

  ; vitamin D intoxication

  ; immobilization

    ; malignancy(esp, bone metastasis)

  ; use of thiazide diuretics

    ; milk-alkali syndrome

  ; sarcoidosis

  ; Williams synd.

           - hypersensitivity to Vit.D

    ; *inadequate phosphate intake in low-birthweight infants

# calcium loading

     1.urinary Na,K excretion 

     2.concentrating ability(  )  polyuria,polydypsia초래

Chapter 51. Magnesium

 major role in cellular enzymatic activity esp)glycolysis,ATPase stimulation

1. body content and distribution of Mg

   : serum Mg;1% of body Mg;1.5-1.8mEq/L

Regulation Of Mg

Intake

      +--1.vit.D

      |  2.PTH

      +--3.increased Na reabsorption

# decrease of Mg absorption 

    calcium

  phosphate

  increased intestinal motility

Renal Excretion

# inhibition of urinary reabsorption

    --> increasing urinary Mg

    ; expanson of ECF volume

  ; osmotic, thiazide, mercurial, loop diuretics

    ; glucagon

    ; *calcium loading

    ; *decreased PTH

Pathophysiologic Conditions

Hypomagnesemia

# ★원인

  malabsorption syndrom

  hypoparathyroidism

  diuretics therapy

  *hypercalcemia

  renal tubular acidosis

  *primary aldosteronism

  alcoholism

  prolonged IV fluid therapy with Mg-free fluids

 early or late neonatal tetany hypoMg 관련있다.

# Clinical Manifestation

    ; *increased neuromuscular irritability

    ; tetany, severe seizure, tremor, personality changes, nausea, anorexia, abnormal cardiac rhythm & abnormal ECGs

# serum Mg level Sx 일치하지 않는 이유

    s-Mg level 항상 body Mg content 반영하는것 아님

     (  predominatly intracellular cation)

    hypomagnesemia Sx Mg depletion 일으키는 primary disease Sx

      비해 minor       

    hypomagnesemia Sx hypocalcemia Sx complicated

# Severe Hypomagnesemia Hypocalcemia 공존이유

    ; *interfere with PTH release & induce skeletal resistance to PTH action

Hypermagnesemia

; >5mEq/L

; 원인

  renal disease

    Mg-containing laxative,enema,IV fluid

  neonates born of mothers who were treated with I.M of Mg sulfate for

     hypertension of pre-eclampsia

  Addison's d's

; Symptoms

    - *hyporeflexia, resp. depression, drowsiness, coma

; Treatment

    - *IV calcium

Chapter 52. Phosphorus

1. body content and distribution of phosphorus

    -intracelluar phosphate;energy 관여

2. regulation of phosphorus

  1) intake & absorption

    (1) diet;milk,milk product,meat

    (2) 흡수;jejunum(dietary phophate 2/3)

          ;vit.D   G.H.

          ;PTH

           alkaline urine

           expansion of ECF

           hyperglycemia

           diuretics

     (3) body reabsorption;   by PTH,1.25(OH)2vitD

                              by thyrocalcitonin

3. pathophysiologic conditions

  1)hyperphosphatemia

         +--hypoparathyroidism

         |  young infant

         |  excessive administration of phosphate

         |  cytotoxic drug

         +--reduction in GFR(25%이하)

  2)hypophosphatemia

         +- starvation

         |  protein-calorie malnutrition

         |  malabsorption syndrom

         |  intracellular shift of phosphate during diabetic ketoacidosis Tx.and

         |    corticosteroid administration

         |  urinary loss 

         |     1'& 3'hyperparathyroidism,renal tubular defect,ECF expansion

         |     diuretic administration

         |  vit.D deficient & vit. D resistant rickets

         |  inadequate intake

         +- prolonged use of phosphate free fluid

         *  Sx ;tissue anoxia

                increased hemolysis

                metabolic encephalopathy;irritability;paresthesia,confusion,seizure

                                           coma

Chapter 53. Hydrogen Ion

Terminology

Normal Acid-Base Regulation

Buffer Systems

; ECF

    - bicarbonate-carbonic acid system

; ICF

    - protein, organic phosphate

; urine

    - mono & di-hydrogen phosphate

# *중탄산염 완충계 & 비중탄산염 완충계

    ; H2CO3+B+Buf- --> B+HCO3 + H+Buf

# Henderson-Hasselbalch equation

    ; *bicarbonate carbonic acid 20:1 되도록 유지

Clinical Acid-Base Relationship

; 3 major components : pH, PCO2, HCO3

Pulmonary Mechanisms

resp.rate () --> CO2 excretion () --> PCO2 () --> pH()

Renal Mechanisms

; *important regulators of acid-base balance in normal condition

; two requirement

    1) prevent loss of bicarbonate

    2) excrete acid equal to daily nonvolatile acid

    - two process

           / filtered bicarbonate proximal tibule에서 거의 reabsorption

           / distal tubule에서 phosphate & ammonia 의해 H+ secetion하면서 HCO3흡수

# Increased H+ Ion Secretion & HCO3 Reabsorption

increased PCO2 

decreased K+ 

reduction in effective arterial blood volume

   (eg,after vomiting or hemorrhage)

administration of mineralocorticoids

# Decreased H+ ion secretion & HCO3 reabsorption 

decreased PCO2 

expansion of ECF volume

inhibition of carbonic anhydrase (e.g. acetazolamide)

cystinosis,heavy metal poisoning with damage to proximal tubule

# distal acidification 장애

intrinsic defect ; 10 distal RTA

20 distal RTA;nephrocalcinosis,vit.D intoxication, amphotericin B administeration

Normal Acid-Base Balance

# ♥신생아에서 ,염기 조절이 힘든 이유

    ; 신장 농축 능력이 낮아서 같은 양의 용질을 배설하는데 많은 물이 필요

    ; 요를 통한 암모니움(NH4+) 배설이 적어 효과적이지 못하다.

    ; 인산염을 소량밖에 배설하지 못해 적정산(titratable acid) 배설능력이 제한되어 있다.

Disturbance Of Acid-Base Balance

★표6-2(p108)

Metabolic Acidosis

# Anion Gap

    ; Na+ - (HCO3 + Cl-)

# Clinical Picture

 deep rapid respiration(kussmaul breathing)

 severe acidosis 의해 peripheral vascular resistance & cardiac ventricular function  

           - hypotension,pulm.edema,tissue hypoxia

# 89 Cause(5)

    ; renal cause

           - proximal form of RTA

           - distal form of RTA

           - CRF

           - low GFR in newborn

    ; other cause

           - diabetic ketoacidosis

           - salicylism

           - severe diarrhea

           - hyperalimentation, lactic acidosis, starvation, poisoning(methyl alcohol or ethylene glycol)

           - inherited aminoaciduria (e.g. methylmalonicaciduria)

           - hypoxemia, shock

Metabolic Alkalosis

# 89 Three mechanism

    excessive loss of H+

           ; prolonged gastric aspiration, persistent vomiting, pyloric stenosis

    increased addition of bicarbonate to ECF fluid

           ; excessive administration(in milk-alkali syndrom)

           ; increased renal reabsorption of bicarbonate caused by

                   - *profound potassium depletion

                   - primary hyperaldosteronism

                   - *cushing syndrome

                   - *bartter syndrome

                   - excessive intake of licorice

    contraction of the ECF volume

# hypokalemia, ECF volume depletion 의한 경우

    - refractory to treatment

    - correction 후에 Tx

# Sx

    ; muscle cramps, weak, tetany (ionized Ca metabolic alkalosis 의해 감소시)

# Laboratory finding

    pH증가, HCO3증가, PCO2증가

  hypochloremia,hypokalemia

  alkalized urine

Potassium depletion, volume depletion 경우에는 다른 Lab/F ?

Respiratory Acidosis

; respiratory distress 함께 hypoxemia 우세한 임상증상

# Acute

    ; neuromuscular disease

        - brain stem injury,G-B synd.,sedative overdose

    ; airway obstruction

         - foreign body, severe bronchospasm, laryngeal edema

    ; vascular disease

         - massive pulm. embolism

    ; other condition

           - pneumothorax, pulm.edema, severe pneumonia

# Chronic

    ; pick wickian synd., poliomyelitis, COPD, kyphoscoliosis, chronic administration of sedatives     

# Lab

; 1.arterial pH 

       2.PCO2 

       3.HCO3;elevated moderately

 -hypercapnia vasodilatation초래   cerebral blood flow(  )  headache & IICP

Respiratory Alkalosis

# ★원인

    ; hyperventilation of psychogenic origin

    ; overventilation of mechanically assisted ventilation

    ; early stage of salicylate overdosage

# Lab

    ; arterial pH 

      PCO2  ,HCO3 

# 임상증세

    ; periorally extremities muscular irritability & paresthesia

           (ionized calcium농도의 감소때문)

 - systemic alkalosis    aciduria

Clinical Assessment Of Acid-Base Disorders

Measurements

# Base excess

    ; 37oc, 40mmHg PCO2에서 strong acid whole blood 적정하여 pH 7.4 하는데 필요한 (mEq/L)

# normal pH ; 7.35-7.45  

# s-carbondioxide cencentration

    ; 25-28mEq/L

  ; 생후 1년간 : 20-30mEq/L

  ; true bicarbonate value보다 1-2mEq/L 높다.

Interpertation

Intracellular pH

 6.8

        [H+] X [total CO2 content in mEq/L]

PCO2 = ------------------------------------

                      25

  pH;7.4,     [H+]=40mEq/L

Cerbrospinal Fluid pH

; bicarbonate-carbonic acid buffer

; CO2 freely diffusible하나 HCO3 slowly change

# Compenasated Metabolic Acidosis

    ; 너무 빨리 교정되면, ECF pH 정상화되나, CSF PH 더욱 감소

Chapter 54. Fluid Therapy

    - daily turnover of water

      +--infant;25% of total body water

      +--adult; 6%  of        

Determination Of Requirement

+--deficit therapy;replace loss of fluid and electrolyte resulting from illness

|  maintenance therapy;replace ongoing normal and abnormal loss of fluid and

|                      electrolyte

+--supplement therapy;in certain disease that require specific fluid

                       and electrolyte

- monitoring of patient

   1)physical examination

   2)determine changes in body weight

   3)frequent review of intake and output

   4)repeated laboratory determinations;

      s-electrolyte,BUN,s-creatine,blood count

Maintenance Therapy

 fluid & electrolyte requirement metabolic rate 직접 연관

 metabolic rate 영향을 미치는 인자

 1) endogenous water production : by oxidation of carbohydrate, fat, protein

 2) urinary solute excretion

 3) heat production

 calorie requirement & maintenance fluid & electrolyte (table 54-1)

 fluid requirement(100cc/100Cal)

 : insensible water loss (1/3), renal water loss(2/3)

 1) insensible water loss증가

   increased activity(30%)

   fever(10 증가시 12%증가)

   hyperventilation

   low birth wt infant

   phototherapy

 2) urinary water requirement 증가

   renal concentrating ability 감소

   ADH분비 감소

 

 urinary water loss 비정상적일시는 maintenance fluid insensible water

 urine output으로 계산

 Na requirement증가

 1) cystic fibrosis(d/t cutaneous loss증가)

 2) salt-losing nephritis, obstructive uropathy, chronic pyelonephritis,diuretic

    therapy (d/t urinary loss증가)

 3) fistula, diversion, NG tube drainage, inflammatory bowel d's(d/t GI loss증가)

    : 대개 isotonic or half saline으로 replacement

 

 

 Na requirement 감소

 1) edematous state d/t hepatic, cardiac, renal ds'

 2) CRF

 3) acute anuric renal failure

 potassium requirement 증가

 1) ongoing GI & genitourinary loss(gastric drainage,laxative,diuretic abuse)

 2) chronic renal ds' with renal medullary injury

 potassium requirement감소

 1) CRF

 2) adrenal insufficiency

 3) acute anuric renal failure

 4) severe acidosis with hyperkalemia

 

 parenteral nutrition

  - maintenance electrolyte in 5% dextrose solution추천

   이유  1.metabolized되는 calorie 25%공급

         2.endogenous protein catabolism 감소

         3.kidney에서 solute load감소시키기 위해

  - 5% dextrose 이상일때

      +--1.hyperglycemia

      |  2.osmotic diuresis

      |  3.intravenous thrombosis

      +--4.infection

  - standard infusate

    성분;crystalline aminiacid solution,20% glucose,various electrolyte,

         multiple vitamin,zinc,copper,chromium,manganese

    투여개요)infusion rate;135ml/Kg/24hr, 120Cal/Kg/24hr

             protein requirement;2.0-3.0g/Kg/24hr

             lipid;20ml/Kg/every 10days

           * peripheral vein 사용시 ex)neonate

              :  glucose concentrate 10%

                 amino acid 30%(30g/L);in older child

                 daily lipid

 TPN complication

     1.sepsis

     2.severe hyperglycemia

     3.profound hypophosphatemia

     4.hyperammonemia

     5.severe metabolic acidosis

     6.electrolyte disturbance

      * very low birth wt infant에서는 Ca, P ratio bone mineralization

        매우 중요

Deficit Therapy

Severity Of Deficit

 : wt loss기준 (table 54-3)

*  Types of dehydration

 

   1) isotonic or isonatremic; Na 130-150mEq/L : 70% of pediatric dehydration

   2) hypotonic or hyponatremic : <130mEq/L

     : hypotonic ECF에서 ICF water shift vol. depletion(ECF)

       circulatory collapse 유발 가능

   3) hypertonic or hypernatremic : >150mEq/L

     : ICF에서 ECF water shift 의한 ICF vol.감소

    * B.Wt 모르는 경우 infant에서 degree of dehydration결정

      1.ant. fontanel

      2.skin elasticity

      3.eyes

      4.Hx of recent pattern of urination

Clinical Manifestation

(table 54-3)

Laboratory Evaluation

   1)hemoconcentration(increased in hemoglobin,hematocrit,and plasma protein)

   2)serum electrolyte

      s-Na water Na와의 상대적인 loss 나타낸다.그러므로 hyponatremic

         dehydration patient에서도 total body sodium 감소되어 있다.

      s-K+

      bicarbonate : acidosis, akalosis, ABGA 도움

   3)BUN,creatine

   4)routine UA

       S.G<1.020 with dehydration시에는 intrinsic renal disease생각

       dehydration mild-moderate proteinuria,hyaline and granular casts,

       white blood cells,occasionally red blood cell contain

   5)anion gap

      [sodium and potassium]-[chloride+bicarbonate]=15  5mEq/L

      증가하는 경우 1.renal disease

                    2.ketosis

                    3.lactic acidosis

Chapter 55. Principles Of Therapy

  * parenteral fluid therapy Ix

     1)severe dehydration

     2)vomiting pt.

     3)profound ongoing loss;diarrhea pt    amounts greater than 100ml/Kg/hr

  * 3 phases

      initial therapy;rapid reexpansion of ECF volume and improve circulatory

            dynamics and renal function

      subsequent therapy;replace remaining ICF and ECF deficit of water

                            and electrolyte

      final therapy;return of pt.'s normal nutritional state and 환자가

                       oral feeding가능할때 시작

Initial Therapy

  goal : ECF rapid expansion

   * solution

       1)metabolic alkalosis(pyloric stenosis);0.9%NaCl in glucose,5g/dl

       2)metabolic acidosis    functioning kidney;H/S

       3)metabolic acidosis without functioning kidney;

             7.5% NaHCO3 28ml to 0.9% NaCl solution 750ml

             and increasing to 1L with 5% dextrose in water

               Na;140mEq,Cl;115mEq,HCO3 25mEq

      - severe dehydrated pt.에서 HCO3대신 lactate or acetate containing solution

           사용시 안좋은점

             ;impaired circulation으로 HCO3 precursor HCO3 쉽게 metabolized

              되지않아 existing acidosis악화됨

     - volume : 20-30ml/Kg,1hr 이내 shock교정안되면 2nd or 3rd dose

                이때는 severely hypokalemia때도 K+ replace안함

     - above Tx shock교정안되면

         1)blood(10mg/Kg) or 5% albumin

         2)other plasma volume expander사용

Subsequent Therapy

: deficit 계속 교정, ongoing loss교정,

                        maintenance fluid & electrolyte

     - urine flow establish s-K+ n'l or slightly low이어도 K+ replacement

      줘야 경우(보통은 치료시작 24시간 후에 한다.)

        1)hypochloremic alkalosis of pyloric stenosis

        2)prolonged diarrhea

        3)diabetic acidosis

Correction Of Deficit

  1) isonatremic dehydration

     (1)external loss of Na from ECF

     (2)movement of Na+ from ECF to ICF to compensate for iontracellular K= loss

     (3)K+ 투여시 ICF sodium 다시 ECF return  ECF volume expansion초래

        ECF Na, & water loss 2/3 교정 ( 24시간동안)

       ) severe,isonatremic dehydration,15% Bwt loss

             deficit;water-150ml/Kg(15% of B.W)

             Na+ :21mEq/Kg

         : 24시간동안 water 100mg/Kg Na14mEq/Kg투여함, 이중에서 20-30ml/Kg of                   sodium 2-3hr 투여하고 나머지는 다음 21-22hr동안 투여한다. 이때 ongoing              normal loss + continuing abnormal loss 교정

            - 24hr 이후

            목표;complete restore of Na + water loss,start replacing K+ loss

            sodium and water requirement = (normal maintenance requirement +25%)

                                            + any ongoing abnormal loss

            K+ loss;replaced over 3-4 days period

             +--K+ concentration < 40mEq/L

             +--rate of K administartion < 3mEq/Kg/24hr

  2) hyponatremic dehydration

        - extra sodium loss = (135-Na) x total  body water (=0.5-0.55xB.W)

          extra-amount 수일에 걸쳐 교정

        - abrupt elevation of s-Na필요한 경우;

           water intoxication Sx(ex.convulsion);s-Na<120

         Tx ; 3% NaCl solution, 1cc/min rate maximally 12cc/Kg of B.W

Hypernatremic Dehydration

# severe hyperosmolarity 인해 cerebral damage

  ; cerebral hemorrhage

  ; thrombosis

  ; subdural effusion

# seizures

    ; frequently during treatment

           - mechanism

                   / cerebral cell during dehydration

                           : increase Na content, increase indiogenic osmoles(esp. taurine)

                     --> rehydration rapid fall in ECF

                     --> excessive water shifting into ICF

                     --> cerebral edema

           - 예방

                   / *10mEq/L/day 이하로 천천히 Na교정

# suitable regimen

    ; 60-75cc/Kg/24hr of 5% D/W 25mEq/L of sodium combination of carbonate & chloride

    ; maintenance ; 3/4 of 유지량 (high ADH level  low urine volume)

       - seizure Tx

            1)3% NaCl 3-5ml/Kg, iv

            2)hypertonic mannitol, iv

# Cx. During Tx

    ; edema, esp. cardiac failure

           - large amount of water with/without salt ECF volume expansion

    ; hypocalcemia

    ; *renal tubular injury with azotemia & loss of concentrating ability

    ; *cerebral edema

           - seizures

           - due to inappropriate and aggressive rehydration

Assessment Of Response

1) clinical

    ; child's cry, degree of activity, skin turgor, blood pressure

2) I/O(stool & urine volume) & B.W

3) urine specific gravity

4) serial serum & urine electrolyte, osmolality, central venous pressure

5) EKG

Chapter 56. Fluid & Electrolyte Treatment Of Specific Disorder

56.1 Acute Diarrhea And Oral Rehydration

   isonatremic dehydration(70%) : rotavirus, non-infectious cause

   hyponatremic dehydration(10%): bacillary dysentery, cholera

   hypernatremic dehydration(20%)

     : home-made high salt solution; boiled skim milk feeding함으로써 renal solute load         증가로 water censerve renal ability 제한되어 질때 fever,high environmental         temparature ,hyperventilation 의해 potentiated 된다.

# IV Therapy Ix

  ; shock

  ; severe dehydration

    ; uncontrolled vomiting

  ; amounts of diarrhea > 100ml/Kg/hr

  ; exreme fatigue, stupor, coma drink 없을때

  ; serious complocation    

           - ex)severe gastric distension

# ORS(oral rehydration solution) composition by WHO(mM/L)

   Table 55-1

    ; other method

       NaCl(0.9% saline solution) 390ml +

    5% D/W 400ml + KCl(2mEq/mL) 10mL +

    NaHCO3(1mg/ml) 30ml + water to 1L

# Oral Rehydration Guidlines

    ; mild dehydration

           - 50ml/Kg of ORS within 4hr

    ; moderate dehydration

           - 100ml/Kg of ORS over 6hrs

    ; 동시에breast feeding or plain water 공급

  ; maintenance therapy

       - 100ml/ORS/Kg/24hr

           - stool volume측정 어려우면 10-15ml ORS/Kg/hr 적당

# Acute Diarrhea초기에도 Oral Feeding 유지 이유

  ; small intestine can absorb various nutrients and up to 60% of food eaten

  ; better weight gain than NPO group

  ; fasting reduce ability of small intestine to absorb nutrients

    ; no physiologic basis for bowel rest during acute diarrhea

      - 대개 NPO for 48hrs with IV therapy시에는 stool 횟수와  

              oral feeding with gastric distension & vomiting(-)

              7-8일이면 usual dietary intake 가능

      - antibiotics Ix

            1.cholera

            2.shigella

            3.amebic dysentery

            4.acute giardiasis

              opiate (intestinal paralysis  )--+infantile diarrhea 도움(-)

              kaolin,pectin(absorbent)       --+

2.diarrhea in chronically malnourished children

      1)s-Na  ,K+  ,Mg  (tetany유발)

      2)s-protein<3.6g/dl

      3)muscle Na+  ,muscle K & Mg  

      4)EKG;tachycardia,low amplitude,flat or inverted T wave

         Cx ; heart failure,lowered cardiac reserve

    - dehydration sign reduced body water에도 불구하고 chronically malnourished

      child에서lower urine osmolarity이유는

       1)relative absence of urea to contribute hypertonic fluid in renal papilla

       2)low dietary protein intak e   tubular conservation of water failure

    - calory supply(vomiting & gatric ditension없을때)

       1)30-40Cal/Kg/24hr,slowly intra-gastric drip

       2)50-100Cal/Kg/24hr & 1-2g protein/Kg/24hr in a few days

       3)250-300Cal/Kg/24hr for suceeding wks iron & copper보충

    - initial parenteral therapy hyponatremic dehydration 준해 solution사용할것

 

   * 1-1.5ml of 50% MgSO4 (4.0mEq/mL)1M q 12hr for 1-3days

       ; severe malnutrition인한 diarrhea 회복되는 동안 일어는 seizure magnesium 반응

    * chronic diarrhea

       고려; 1)cow's milk protein allergy

             2)specific disacharidase def.(acquired;lactose)

3.congenital alkalosis of G-I origin

     congenital defect in chloride transport in small & large bowel

      ;pyloric stenosis 비슷하게 치료

 

4. Pylroric stenosis

     특징;  1)되도록 빨리 KCl 투여 (urination하자마자)

            2)relatively more Na + K 투여 as chloride salt

              +--  1. large deficit of chloride

              +--  2. some correction of alkalosis as volume is expanded

 

         paradoxic aciduria with alkalosis K+ depletion의심

               repletion potassium amount 증가시킴, 대개 12hr내에 교정

     * delay operation for at least 36-48hr

          : optimal adjustment of body functions

            1)adequate fluid Tx

            2)stomach decompression

5. fasting and thirsting

  * Tx ; isotonic solution +--rapid ECF expansion

                           +--improve renal function        

    child,adult infant 비해 given degree of dehydration 1/3-1/4 water & Na 적게          투여

6. Electrolyte disturbances associated with central nervous system disorders

    : 종종 sodium conc. 이상을 초래 (hyponatremia)

      1)surgical or  traumatic damage of brain,encephalitis,bulbar poliomyelitis,

         CVA,4th ventricle tumor,subdural hematoma  Na urine loss

      2)SIADH : neonatal hypoxia, hydrocephalus urine Na증가 (20meq/L)

      3)acute symptomatic hyponatremia치료

        : prompt hypertonic saline furosemide

      * chronic asymptomatic hyponatremia : water restriction

7. preoperative,intraoperative, and postop. fluids

  - 목적;supply carbohydrate to ensure adequate glycogen storage

  - vomiting 없는 small infant operation 3시간 전까지는 P.O.

  - intestinal obstruction high bilirubin발생

  - hypoprothrombinemia ; vit.K1 1mg I.M

  - over administration of fluid ; most common error

  - K+ 주지 말것

    1)extensive tissue trauma or anorexia intracellular K+ 많은 양이 release

    2)shock acute renal loss 합병되어 hyperkalemia 치료 더욱 어렵다.

  - postop intake limitation for 24hrs

    water intake ;85ml  /100Cal

          (  antidiuretics from trauma or circulatory readjustment)

Isolated Disturbances In Blood Ph And Concentrations Of Electrolytes

Acidosis

    (1)respiratory acidosis

      Tx;assisted ventilation

    (2)metabolic acidosis

     :lactic acidosis,glycogen disorder,circulatory insufficiency,hypoxiaEosms sodium        lactate 적절하게 metabolized안될 있다. 그러므로 이때에는 sodium bicarbonate

      1-2mEq/Kg투여

     - 필요한 bicarbonate(mEq);Astrup

       소요량 of bicarbonate= (-BE) x B.W. x0.3

       0.5ml/Kg of sodium bicarbonate ; s-HCO3 1 mEq/L

     - acidosis 인한 Sx 현저할때를 제외하고는 s-bicarbonate level 15 mEq/L이상으로          올리려고 필요없다.

      (  overcorrecting acidosis tetany 초래)

       underlying cause Tx 필요

Alkalosis

    (1)metabolic alkalosis

     -경우 administration of excess amount of alkali

           loss of H+ ion

           volume contraction with disproportionate loss of Cl-

           severe hypokalemia

     -severe alkalotic therpy

        Tx;ammonium chloride;/d(0.2-0.3)

     a)metabolic alkalosis with volume contraction

       urine chloride < 10mM/L

        경우;vomiting,gastric suction,congenital chloridic diarrhea,dietary

             chloride def,diuretic administration

        Tx;volume expansion with K,Cl deficit replace

     b)chloride-resistant

       urine chloride > 15mM/L

       경우;hyperadrenalism

            Bartter syndrom

            severe K+ depletion

            licorice ingestion

    (2)respiratory alkalosis

      경우; salicylate intoxication

            CNS disease such as, trauma,infection,tumor

            fever or anxiet

            CHF

            hepatic insufficiency

            gram-nagative septisemia

         Tx;underlying cause

Hyponatremia

1)asymptomatic hyponatremia

  Tx;fluid restriction   water overload 의한 경우

  -urine Na<10mEq/L경우

    sodium depletion

    nephrotic syndrom

    CHF

    hepatic failure

  -urine Na=50mEq/L

    expansion of ECF with water

    renal tubular injury

2)symptomatic hyponatremia

  hypertonic saline solution

Na mEq required=(Cd-Ca) x 0.- 0.7 x B.W

   12mEq/Kg of 3% NaCl(6mEq Na/Kg) s-Na 10mEq/L 올린다.

   s-Na증가는 5-10mEq/L over 1-4hr 소량씩

Hypernatremia

brain cell로부터 water shift

  subdural,subarachnoid,intracerebral hemorrhage초래

; high mortality, esp, if exceeds 158 mEq/L

# Treatment

    ; IV fluid consist of glucose in water, potassium acetate, calcium

    ; *peritoneal dialysis

Hypokalemia

경우 1)primary hyperaldosteronism

     2)Bartter syndrome

     3)congenital alkalosis of G-I origin;KCl loss

     4)thiazide & loop diuretics(lasix)

severe hypokalemia

    skeletal muscle weakness

    peristalsis

    ileus

    inability to the kidney to concentrate urine

# Treatment

    ; *up to 3mEq/kg/24hr

    ; in bartter syndrome

           - 10 mEq/kg/24hr

           - indomethacin

    ; in Gitelmans syndrome

           - MgCl2

Hyperkalemia

# K+ > 6.5meq/L Tx. Promptly

  all K+ intake discontinue

  sodium bicarbonate IV rapidly

           ; 1-3mEq/Kg over 5-10min

  glucose & insulin

           ; 0.5 -1g of glucose/Kg with 1 unit crystalline insulin/g of glucose over 2hr period

  IV calcium gluconate

           ; 0.5ml of 10% solution/Kg over 2-4min

    ;potassium cardiac toxicity 맞서기 위함

  *kayexalate 1g/Kg/24hr p.o or enema every 6-12hr

  hemodialysis,peritoneal dialysis

Hypomagnesemia

 <1.3mEq/L latent or manifest tetany

경우   chronic diarrhea or vomiting

        sprue

        celiac disease

        prolonged parenteral fluid Tx

        hyperaldosteronism

        infantile tetany(transient hypoparathyroidism)

Tx; 0.1ml of 24% solution MgSO4(0.2mEq/Kg, q 6hrs)

     3mEq/L Mg to maintenance fluid

Hypermagnesemia

; >10mEq/L

  drowsiness

    coma

  abolished DTR 

  respiratory depression

  atrioventricular or intraventricular conduction defect

# 원인

    ; ARF, addison disease, iatrogenic(using Mg in treating toxemia of pregnancy)

# Treatment

    ; *IV calcium gluconate

56.9 Tetany

; state of hyperexcitability of the CNS & PNS

; ★경우

    - decrease of H+

    - decrease of Ca++

    - decrease of Mg++

; Ca++ in normal albumin

    - 40-50% of total calcium

    - 4.0-5.2mg/dl

    - *albumin 1g/dl : calcium 0.8mg/dl 비율로 감소

    - tetany develop at Ca++ < 3.0mg/dl (total Ca<7.0mg/dl)

           / *almost alway develop at Ca++ < 2.5mg/dl (total Ca<5mg/dl)

; normal serum Mg

    - 1.6-2.6 mg/dl(75% Mg++)

  - *tetany develop at Mg++ < 1.0mg/dl

Manifest Tetany

; carpopedal spasm - wrist & ankle M. spasm

; laryngospasm

    - vocal cord spasm

           --> inspirtory obstruction

           --> high pitched insp. crow

; paresthesia

    - numbness & tingling sense of hand & feet

; convulsion

    - *infant에서 nervous system hyperexcitability 유일한 증거

Latent Tetany

; induction of manefest tetany by ischemia, mechanical, electrical stimultion

; Trouseau Sign

    - B.P cuff arm 대고 systolic B.P 상방에서 3분간 inflate시켜 동맥순환을 못하게 하여 carpopedal spasm 유발

; chvostek sign

    - external auditory meatus 전방을 tapping하여 facial n. 자극하여 upper lip or entire mouth twitch orbicularis oris contraction 유발

; peroneal sign

    - fibular head tapping foot dorsiflexion & foot abduction 유발

; Erb sign

    - positive response of motor nerve to electrical stimulation less than normal state

; prolonged Q-T interval 

Alkalotic Tetany

; very rare

; be induced through spontaneous overventilation,producing resp. alkalosis

; Treatment

    - rebreath into a bag or baloon to increase PCO2 

Hypocalcemic Tetany

Disorders Of Parathyroid Function

# neonatal hypocalcemia

    (=transient physiologic hypoparathyroidism of the newborn)

    ; *common

    ; ♥기전

           - physilogically inactive parathyroid gland failing to respond to low Ca++ concentrattion

           - partial refratoriness of target cell to PTH in newborn

           - *excessive thyrocalcitonin secretion

                   / *major factor of persistent hypocalcemia in pemature infants

           - inadequate intake of vitamin D & little exposure to sunshine

           - *physiologic mild maternal hyperparathyroidism

                   / hypercalcemia of fetus

                           --> *inhibition of the fetal parathyroid

Early Hypocalcemia

    ; during first 72hr, before significant oral intake

    ; High Risk Group

           - LBW with IUGR

    - infants born of diabetic mother

    - infants of prolonged difficult labor

           - infant of mother with adenoma

           - infant with familial hypoparathyroidism

    ; premature infant with RDS

           - *extremely high incidence

           - 이유

                   / low calcium intake, increased endogenous phosphate from catabolism

                   / receive sodium bicarbonate

    ; asymptomatic hypocalcemia of premature infant

           - usually spontaneous recovery

           - *oral calcium gluconate으로 치료를 한다.

Late Hypocalcemia

; during first 5-10days

; high phosphate milk

    - *common cause

; 기전

    - high phosphate food(e.g. cow's milk) intake & relatively high tubular reabsorption & low GFR

           --> elevated serum phosphate

           --> decrease calcium level through depositon of calcium phosphate

           --> poor response of infant parathyroid gland

           --> progressive hypocalcemia

Clinical Manifestation

    ; *convulsion

           - important

    ; carpopedal spasm - rare, chvostek sign - common

           - infant에서는 no sing of tetany

    ; laryngospasm

    ; *irritability, muscular twitching, tremor, jitteriness

           - common in newborn

    ; nonspecific symptoms

           - poor feeding, vomiting, lethargy

    ; prolonged Q-T

Diagnosis

    ; s-Ca < 7mg/dl

           - < 7.5mg/dl : suggestive

Treatment

# convulsing infant

  ; 10% ca-gluconate 2ml/kg slowly I.V

    ; repeat bolus at 6-8hr interval or continous infusion (50-75mg elemental Ca/Kg/24hr)

# oral calcium gluconate or lactate

    ; calcium latate 선호

    ; *1-3일후에야 normal calcium level

    ; 최소한 1주일 투여

    ; calcium lactate powder (13%) : 100mgCa++/770mg

           - *Ca : P=4 : 1

    ; normal serum calcium되면

           - reduced calcium supplement in steps

    ; in most infants, normal calcium homeostasis & normal parathyroid responsiness in 1-2wks

    ; 호전이 안되면

         - congenital hypoparathyroidism, vit.D def., absorptive or metabolic abnormalities of vit.D 의심

Congenital Absence Of The Parathyroids

    DiGeorge synd.    +--)aplasia of thymus

                      |  )abnormalities of great vessels of heart

                      +--)isolated parathyroid aplasia

                     Tx; )dihydrotachysterol 0.05-0.1mg/day

                         )1,25(OH)2vitD3  0.25-0.5 ug/day

Hypocalcemia & Tetany Caused By Vit.D Def. Or Abnormalities Of Vit.D Metabolism

   -onset;)vit.D def. mother breast feed

          )failure of normal vvit.D metabolism

             neonatal hepatitis,cytomegalic inclusion d's,biliary atresia

          )vit.D-dependent (pseudodeficient) rickets ; kidney에서 1-hydroxylation                     장애

               )steatorrhea due to pancreatic lipase def. or intrinsic intestinal                          mucosal disorder

               )large combined anticonvulsant;phenobarbital, diphenylhydantoin,primidone  

Hypomagnesemic Tetany

       transient physiologic hypoparathyroidism of newborn

          : hypomagnesemia, hypocalcemia, hyperphosphatemia : Tx. Mg 공급

       prolonged Mg-free parenteral nutrition

       renal tubular dysfunction or nephropathy(aminoglycoside, cisplatin사용)

       intestinal malabsorption