Metabolic, volume and ion disturbances. Salty pickle with a hint

of sugar.

KANIZSAI PÉTER - BERÉNYI TAMÁS

BUFFERS

METABOLIC ACIDOSIS

pH < 7,35

CO2

HCO3 < 22

+/+

+/-

O2/sat

ANION GAP (6-12 mEq/L)

nature.com

A decreased anion gap (< 6 mEq/L) may suggest the

following:[4]

Hypoalbuminemia

Plasma cell dyscrasia

Monoclonal protein

Bromide intoxication

Normal variant

A normal anion gap (6-12 mEq/L) may indicate the following:[4]

Loss of bicarbonate (ie, diarrhea)

Recovery from diabetic ketoacidosis

Ileostomy fluid loss

Carbonic anhydrase inhibitors (acetazolamide, dorzolamide, topiramate)

Renal tubular acidosis

Arginine and lysine in parenteral nutrition

Normal variant

An elevated anion gap (>12 mEq/L; “mud pilers”) may indicate the following:

Milk-alkali syndrome

Uremia

Diabetic ketoacidosis

Propylene glycol

Isoniazid intoxication

Lactic acidosis

Ethanol ethylene glycol

Rhabdomyolysis/renal failure

Salicylates

HIPERNATRAEMIA HIPEROZMOLARITY VOLUME OVERLOAD (FREE WATER!) WIPLASH ALKALOSIS HIPOKALAEMIA DECREASED OXYGEN DOWNLOAD (LEFT SHIFT) INCREASED LACTATE PRODUCTION INTRACELLULAR ACIDOSIS CSF ACIDOSIS HYPERCAPNIA

METABOLIC ACIDOSIS

INCREASED ANDOGENOUS HYDROGEN ION PRODUCTIONEXOGENOUS ACID LOAD

HYDROGEN ION ORIGINATING FROM INCREASED PROTEIN INTAKE AND EXCEEDING EXCRETORY LIMITS

RENAL BICARBONATE LOSS

RENALLY COMPENSATED RESPIRATORY ALKALOSIS

DECREASED MYOCRDIAL CONTRACTILITY

DECREASED SVR (ARTERIOLAR DILATATION/VENOUS CONSTRICTION)INCREASED INOS SYNTHESIS

CENTRALIZED BLOOD VOLUME – IMPAIRED SPLANCHNIC CIRCULATION

PULMONARY VASOCONSTRICTION

HYPERVENTILATION (FATIGUE)INCREASED METABOLIC RATE (DECREASING ATP AND 2-3 BPG LEVELS)HYPERGLYCAEMIA AND HYPERKALAEMIA

AMS (CONFUSION)SIRSCELL MEMBRANE ION PUMP DEFICIENCY

METABOLIC ACIDOSIS

METABOLIC ACIDOSIS

H+ /NORMAL PCO2

RENAL FAILURE?DIABETES MELLITUS?

POISONONG?(SALICYLATE; ALCOHOLS;

PARACETAMOL)

ANION GAP

MEASURE CHLORINE - CALCULATE!

HIGH NORM / LOW

MEASURE LACTATE!

HIGH NORM / LOW

HYPERCHLORAEMIA

↑K+ NORM/ K+

PERFUSION DEFECT, PIOSONING*

CONGENITAL CAUSE

ALCOHOLIC

KETOACCIDOSIS

RHABDOMYOLYSIS

EARLY AKIHIPOALDOSTERONISM

ACID INPUT

HYPERALIMENTATION

RENAL TUBULAR ACIDOSIS

TUBULAR DAMAGE

DIARRHOEA

CURED DKA

Hyperkalaemia

High potasiumlevels

„PSEUDO” CONTROL

INCREASED INTAKE

DIRET POTASSIUM

BLOOD

ICF SHIFT TO ECF ACIDOSIS

SEVERE CATABOLISM

RHABDOMYOLYSIS

K-SPARING DIUR. CELL/TISSUE DAMAGE

MINERALOCORTICOID

DISTURBANCE

DRUGS: (ALDOSTERON

ANTAG.; DIGITALIS INTOX.; SCOLINE, ßBLOCKER….)

HYPEROSMOLARITY

DECREASED EXCRETION

AKI TUBULAR DISEASES

OLIGURIA

HYPOALDOSTERONISM

MEDS (K-SPARING

DIURETICS; CYCLOSPORIN; ACEI; NSAID)

INTRACELLULAR POTASSIUM

(MUSCLE)SERUM POTASSIUM↑

(BLOOD)CALCIUM ENTRY

(HEART MUSCLE)

CALCIUM GLUCONATE

(1-5 PERC)

BICARBONATE

(5-10 MIN)INSULIN+SUGAR

(30MIN)RRT

(MINUTES)…. FRUSEMIDE

Hypokalaemia

ARTEFICIAL (SMALL ANION GAP) METABOLIC / ENDOCRINE

HYPERNATRAEMIA DIABETES INSIPIDUS OR DIABETIC COMA HYPERPARATHYROID STATES METABOLIC ACIDOSIS RENAL TUBULAR ACIDOSIS

GASTROINTESTINAL VOMITING PROLONGED DIARRHOEA KIDNEY DISEASE LOSS OF PANCREATIC JUICE (FISTULA)

MIDBRAIN INJURY (NEUROGENIC HYPERVENTILATION)

DRUGS ANDROGENES OESTROGENES STEROIDS DIURETICS (CARBONIC ANHYDRASE -

INHIBITOR)

HYPERCHLORAEMIA

se. Cl > 106 mEq/L

pH <7.35CO2< 22 mEq/L.

METABOLIC ALKALOSIS

DIARRHOEA

VOMITING

NG TUBE

HYPONATREMIA

SUPRARENAL CORTICAL INSUFF.(ADDISON)RENAL FAILURE

OEDEMA – COMGESTIVE HEART FAILURE

PSEUDOHYPONATREMIA

SALT LOOSING NEPHRITIS

INFUSION THERAPY

SWEATING

BURNS

DIETARY PROBLEMS

DRUGS

LOOP DIURETICS

ALDOSTERONE

ACTHCORTICOSTEROIDS

BICARBONATE

LAXATIVES

GENETIC DISEASES

CYSTIC FIBROSIS

BARTTER’S SYNDROME

HYPOCHLORAEMIA

se. Cl < 98 mEq/L

pH >7.45CO2> 32 mEq/L

se.osmol < 280 mOsmol/L

DEHYDRATION SYNDROMES (VOMITING) LOW CHLORINE LEVELS MUSCLE SPASTICITY TETANY SUPERFICIAL BREATHING HYPONATREMIA WEAKNESS MUSCLE TWITCH SEWATING FEVER

NAUSEA AND VOMITING HEADACHE CONFUSION (AMS) FATIGUE WEAKNESS RESTLESSNES, AGITATION MUSCLE WEAKNESS, SPASMS CONVULSIONS OBS COMA

HYPONATRAEMIA

seNa < 135mEq/L

Serumosmolarity

280-295mOsmol/LISOTONIC

>295mOsmol/LHYPERTONIC

<280mOsmol/LHYPOTONIC

Urineosmolarity

<100mOsmol/L„WATER

INTOXICATION”

>100mOsmol/LRENAL

seNa < 135mEq/L

HYPERVOLAEMIA

Urine Na

NORMOVOLAEMIA

> 20 mEq/LRENAL LOSS

HYPOVOLAEMIA

Urine Na Urine Na

< 10 mEq/LEXTRARENAL

> 20 mEq/LRENAL

< 10 mEq/LOEDEMA*

*HEART FAILURECIRRHOSISNEPHROSIS SY.

POTASSIUM DEPLETION

SIAD OSMOSTAT ENDOCRINE*

*HYPOTHYREOIDGLYCOCORTICOID

SIAD

SIAD

Na

HYPERNATRAEMIAHYPERNATRAEMIA IS SUCH ANHYPEROSMOLAR STATE WHERE THEDECREASE OF TBW IS DISPROPORTIONATETO THE ION CONCENTRATION – IT IS REALLYA „WATER-PROBLEM” RATHER THAN ANION DISTURBANCE

PATHOPHYSIOLOGY OF HYPERNATRAEMIA TÜNETCSOPORTOK

COGNITIVE DYSFUNCTIONS ASSOCIATED WITH NERVE CELL SHRINKING

LETHARGY, OBTUNDATION, CONFUSION, CONVULSIONS, NYSTAGMUS, MYOCLONUS, IRRITABILITY

THE CLNICAL PROCESS OF DEHYDRATION ORTHOSTATIC DECREASE IN BP, TACHYCARDIA, OLIGURIA, DECREASED SKIN TURGOR

OTHER ASSOCIATED PROBLEMS WEIGHT LOSS, GENERAL WEAKNESS

1. HYPOTONIC FLUID LOSS (WATER AND ELECTROLYTE LOSS)2. PURE WATER LOSS3. USE OF HYPERTONIC SALINE

TO ESTABLISH THE DIAGNOSIS: ELECTROLYTE LEVELS (NA+, K+, CA2+ ) BLOOD SUGAR CN, CREATININ URINE ELECTROLYTES (NA+, K+) URINE AND PLASMA OSMOLARITY 24 HR COLLECTED URINE PLASMA AVP/COPEPTIN LEVEL (IF REQUIRED)

HYPERNATRAEMIA

Diabetes insipidus

Central diabetes insipidus

Renal diabetes insipidus

Polydipsia-polyuriasyndrome

State-of-the art diagnosis:

1. Stimulation of AVP release via a water deprivation test

2. Indirect measurement of AVP release by monitoring of

urine osmolality and volume during water deprivation (ability

to concentrate urine).

3. Additional desmopressin administration to differentiate

nephrogenic DI from central DI.

Direct AVP measurement therefore is not the diagnostic

reference standard because of its methodological limitations

(instability of analyte and uncomfortable assay handling)

Differential Diagnosis of Diabetes insipidus

CT-proAVP (hs Copeptin)

Suspicion of diabetes insipidus

with polyuria-polydipsia syndrome

CT-proAVP basal

(in the morning, fasting, after 8h dehydration)

CT-proAVP

<2,6 pmol/L

CT-proAVP

>20 pmol/L

Central Diabetes

insipidus totalis

Renal Diabetes

insipidus

CT-proAVP

>=2,6 - 20 pmol/L

CT-proAVP-Index

<20

CT-proAVP-Index

>=20

Central partial

diabetes insipidusPrimary

polydipsia

Ratio of CT-proAVP-Delta (8 to16h)

and Serum-Na+ (16h) = CT-proAVP-Index

The available data demonstrate limitations of current biochemical tests

for the differential diagnosis of DI, potentially leading to incorrect diagnosis

and treatment. The newly available assay for C terminus of the vasopressin

precursor, holds promise for a higher diagnostic specificity and simplification

of the differential diagnostic protocol in DI.

Advantages for the diagnostic routine with CT-proAVP

• Significantly higher diagnostic accuracy for all variations of diabetes

insipidus and primary polydipsia

• Considerably eased differential diagnosis of polyuria-polydipsia

syndrome

• Reduced physical and psychological exposure of the patient due to

simplified WDT and redundancy of desmopressin stimulation

• Support of safe therapeutic decisions with highly sensitive

measurement values

• Overall cost reduction due to reduced complexity, less lab consulting

and no prescription of desmopressin

WHAT FLUID? IN OLIGURIA, HYPOTENSION: 0,9 % NACL

NORMOTENSION: D5W

HOW FAST ? HALF OD THE DEFICIT OVER 24 HRS

THE REST OVER 24-48 HRS

METABOLIC ALKALOSIS

H-ION LOSSH-ION TRANSFER TO IC VOLUMEEXOGENOUS ALKALICONTRACTION ALKALOSIS

HyPOKALAEMIA!- I.C. H-ION SHIFT → INCREASED

BICARB. REABSORPTION

RESPIRATORY ALKALOSIS

CENTRAL

PATHOLOGY(RESP. CENTRE)

TRAUMA

TUMOR

STROKE

DRUGS

HYPOXIA INDUCED

HYPERVENTILATION

PULMONARY

PATHOLOGY

PEPNEUMONIA

ASTHMA

PULM. OEDEMA

JATROGENIC

HYPERVENTILATION

WEAKNESS, MYALGIA, POLYURIA, ARRHYTMIASHIPOVENTILATION SYMPTOMS OF HYPOCALCAEMIA

AFFECTED ORGANS

CNS

INCREASED

NEUROMUSCULAR

ACITIVITY

DECREASED ICP DECREASED

RESPIRATORY TRIGGER

CIRCULATION

ARRHYTHMIAS

DECREASED

CONTRACTILITY

DECREASED CEREBRAL

PERFUSION

OTHER

HB. DISSOC. CURVE LEFT

SHIFT

HYPOKALAEMIA

RESPIRATORY ACIDOSIS

INADEQUATE ALVEOLAR

VENTILATION

CENTRAL RESPIRATORY DEPRESSION: DRUGS, TRAUMA, BLEEDING, OBESITY

NEUROMUSCULAR DISORDERS: GBS, MG, ORGANOPHOSPHATE, MYOPATHIES

LUNG OR CHEST WALL ABNORMALITIES: CHEST TRAUMA, PTX, HTX, COPD ACUTE

EXACERB., PULM. OEDEMA, ARDS

AIRWAY OBSTRUCTION

OTHERS: INADEQUATE MECHANICAL

VENTILATION

EXOGENOUS CO2 LOAD

INTOXICATION,REBREATHING

CO2 OVERPRODUCTION

MALIGNANT HIPERTERMIA

CHRONIC RESPIRATORY ACIDOSIS

PH NORMAL

PCO2 ↑↑PO2 ↓

DANGERS OF O2

THERAPY!

PINK PUFFER VS BLUE BLOATER

CAPILLARIS MEMBRAN

CELLULARIS MEMBRAN

kOLLOID

SA / RINGER

5% DEXTROSE (DEST.VÍZ)

VOLUME STATE

HYPOVOLAEMIA NORMOVOLAEMIA HYPERVOLAEMIA

CAUSE AND EXTENT OF FLUID LOSS

(QUALITATIVE/QUANTITATIVE)

FLUID REPLACEMENT CRYSTALLOID

COLLOID

BLOOD PRODUCTS

VOLUME STATE REASSESSED

NORMÁL SZISZTOLÉS FUNKCIÓ

GYENGE SZISZTOLÉS FUNKCIÓ

VERŐVOLUMEN

ELŐTERHELÉS/VOLUMENVOLUMEN

DISTRIBUTES IN THE WHOLE ECV

SAME COMPOSITION AS OF THE INTERSTITIAL FLUID

SAME OSMOTIC PRESSURE AS OF THE PLASMA

MIGHT CAUSE TISSUE OEDEMA

MIGHT CAUSE ACIDOSIS IN HIGH QUANTITY

CRYSTALLOIDS

SOLUTIONS CONTAINING MACROMULECULES

REMAIN IN THE INTRAVASAL SPACE AND BIND WATER

IF COLLOID OSM. PRESSURE = PLASMA OSM. PRESSURE ISOVOLAEMIC HAEMODILUTION

IF COLLOID OSM. PRESSURE = PLASMA OSM. PRESSURE → HYPERVOLAEMIC HAEMODILUTION

COLLOIDS

PLAZMA SA RINGER RL HALF

NORMAL

RD BALANCE

OSMOLARITY 288 312 150 426

PH 7,4 5-7 5-7 3-6

GLUCOSE 5 5%

NA 140 147 130-140

K 4,2 4,0 4,5-5,0

MG 3 0-3

PHOSPHATE 1,25

CL 103 155 96-109

LACTATE 1-1,5 0-29

ACETATE - 0-27

NA:CL 1,36

PLAZMA SA RINGER RL HALF

NORMAL

RD BALANCE

OSMOLARITY 288 308 312 150 426

PH 7,4 4,5-7 5-7 5-7 3-6

GLUCOSE 5mmol 5%

NA 140 154 147 130-140

K 4,2 4,0 4,5-5,0

MG 3 0-3

PHOSPHATE 1,25

CL 103 154 155 96-109

LACTATE 1-1,5 0-29

ACETATE - 0-27

NA:CL 1,36 1

PLAZMA SA RINGER RL HALF

NORMAL

RD BALANCE

OSMOLARITY 288 308 312 300 150 426

PH 7,4 4,5-7 5-7 5-7 5-7 3-6

GLUCOSE 5mmol 5%

NA 140 154 147 131 130-140

K 4,2 4,0 5,4 4,5-5,0

MG 3 0,5 0-3

PHOSPHATE 1,25

CL 103 154 155 112 96-109

LACTATE 1-1,5 27 0-29

ACETATE - 0-27

NA:CL 1,36 1 1,17

VOLUME OVERLOAD

ALLERGIC REACTION

ACIDOSIS

pH 4,5-7

Na 154Cl 154

STRONG ION DIFFERENCE

COAGULOPATHY

J.TRAUMA – 2011.

PRIMARY DAMAGE

SECONDARY DAMAGE

VARIABILITY

OUTCOME

THE CAPACITY OF A SHIP TO ABSORB DAMAGE AND MAINTAIN MISSION INTEGRITY

COAGULOPATHY

HYPOTHERMIA

ACIDOSIS

URINE OUTPUT

URINE SODIUM AND OSMOLARITY

MAP (CPP AND APP) BUN SVIHR LACTATE(CLEARANCE) PH, BE, HCO3

SMVO2, OR SCVO2

PCO2

TISSUE PCO2 (SUBLINGUAL, GASTRIC) EXTRAVASCULAR LUNG WATER (EVLW) INTRA-ABDOMINAL PRESSURE (IAP)…

26 YEAR OLD GUY WORKS ON A BUILDING SITE IN HOT WEATHER. COMPLAINS

OF NAUSEA AND WEKANESS. HE IS OFFERED FLUIDS BUT REFUSES IT BECAUSE

OF FEAR FROM VOMITING. IN TWO HOURS HE LOSES CONSCIOUSNESS AND AN AMBULANCE TAKES HIM TO

THE ED. S

BOTHERWISE HEALTHY, DRUG ALLERGY: PENICILLINTHIS IS DAY 3 ON THE BUILDING SITE, BUT GETS EXHAUSTED VERY EARLY

THE TEMP IS 37 °C IN SHADE.

A

R

LOOK, LISTEN AND FEEL!POCTBLOODSIMAGING

CTAS/HUTASSUGGESTED THERAPYTHERAPEUTIC END POINTS

ADRY, WARM AND PALE SKIN. GCS: 14/15. RR:110/70, P: 134/MIN, SPO2: 94 %PH:7,51, PCO2:49 HGMM, PO2:85 HGMM, BE:5, NA:159, K:3,0, HCO3: 29, LACTATE: 1,9, SAO2: 96 %CN: 11, CREAT: 112, INR:1,09, FBC: RBC:5,8, HT:0,54, HB:168, WCC:8,9, PLT:198

19 YEAR OLD KNOWN T1D PATIENT IS TRANSFERRED TO THE ED. SHE IS

UNCONSCIOUS. S

BSHE’S BEEN DIABETIC SINCE THE AGE OF 10 AND HER DIABETES IS QUITE

BRITTLE. SHE IS VERY THIN, BMI:17. NKDA.ACCORDING TO HER MOTHER SHE’S BEEN HAVING A TEMP FOR DAYS, SHE HAS

ACHEST COUGH, AND YELLOWISH SPUTUM. SHE ATE LESS AND THEREFORE

HALVED HER USUAL DOSE OF INSULIN.

A

R

GCS:1-T-4, NO NEURO DEFICIT. RR:80/50 HGMM, P:125/MIN, SPO2: 78 % (FIO2:0,21)PH:6,97, PCO2:17, PO2:61, BE:-19, NA: 132, K:5,7, HCO3:14, LACTATE: 2,8, SAO2:78 %OTHER BLOODS: BUN: 17, CREAT:132, INR:1,25, FBC: RBC:4,2, HT:0,48, HB: 148, WCC:22.000, PLT: 98, PCT:3,8

CTAS/HUTASOTHER INVESTIGATIONS

SUGGESTED THERAPY

THERAPEUTIC ENDPOINTS

PREGNANCY

BICARB < 5 MMOL/L

PH< 7.1 HYPOKALAEMIA (<3.5 MMOL/L) GCS < 12 SPO2 < 92 % ANION GAP > 16 SBP < 90 HGMM / 60> BPM < 100

BLOOD SUGAR > 11MMOL/L

BICARBONATE (HCO3) < 15 MMOL/L

(VENOUS) PH < 7.3

HYPERGLYCAEMIA

METABOLIC

ACIDOSISKETOSIS

DKA

UNCONTROLLED DM HYPEROSMOLAR STATE

STRESS (HYPERGLYCAEMIAA)

LACTATE ACIDOSIS

HYPERCHLORAEMIC ACIDOSIS

URAEMIA

SALICYLATE (!)

ALCOHOL

HYPEREMESIS

KETOTIC HYPERGLYCAEMIA

FASTING

IV ACCESS

0.9% NACL - 1000ML/HR

INSULIN + 500ML + 2G KCL/HR

POCT ABG (PH; BICARB) BLOOD SUGAR

ANION GAP

ELECTROLYTES (VOLUME STATE) URINE (KETON)

START INZULIN

SHORT ACTING IV (4-6U/H)

MONITORING

LEVEL OF CONSCIOUSNESS (GCS – IF REQUIRED MECH. VENT.) CVP / VOLUME; SCVO2 .... ECG, IABP …. PERFUSION

UOP

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