electrolytesandacidbase - nigel fong · hyponatremia–pathophysiologic* ... malignancy*...

Electrolytes and Acid Base

Yii Zheng-‐Wei

Normal ECF Osmolarity Regula>on -‐ Input

Normal ECF Osmolarity Regula>on -‐ Output

Regulators of ADH

Symptoms of sodium disorders

•  CNS – Limited intracranial space – Fa>gue – Headache – Nausea/Vomi>ng – Confusion – Seizures – Coma

Hyponatremia – Pathophysiologic Approach

ADH High ADH Low

Chronic Low BP SIADH Endocrinopathy

Volume Deple>on (Clasically Diure>cs/Osmo>c Diuresis/GI

Loss)

Malignancy Hypothyroidism (Crazy rare)

Advanced Renal Failure

Heart Failure CNS bleeds Primary Polydipsia (Generally psych

pa>ents)

Cirrhosis Lung Low-‐nutrient diet

Nephro>c Syndrome Drug SE

Adrenal Insufficiency Pain

Cerebral Salt Was>ng

Reset Osmostat

Hyponatremia – SIADH E>ologies 1.  Malignancy –  Classically Small Cell Lung CA (Make loads of

hormones) 2.  CNS Bleed 3.  Lung pathology –  Classically Pneumonia (though how common it is I

don’t know) 4.  Drugs –  Centrally ac>ve stuff (an>epilep>cs, SSRIs etc.)

5.  Pain

Hyponatremia – SIADH Diagnos>c Criteria

1.  Low Serum Osmolality (<275mOsm/Kg) 2.  Urine Osmolality >100mOsm/kg with hypotonic

serum 3.  Urine Sodium >40mmol/L with normal salt intake 4.  Normal thyroid and adrenal func>on 5.  Addi>onal features

1.  Serum urea <3.6mmol/L 2.  Low serum crea>nine 3.  Serum uric acid 4.  Abnormal water loading test (excre>on of less than 80%

of a 20ml/Kg water loading in 4 hours)

Hyponatremia – Clinical Approach Urine Sodium

Volume Status Low High

Hypovolemic 1.  Actual Hypovolemia (usually GI Loss)

1.  Diure>cs 2.  Primary Adrenal

Insufficiency

Euvolemic 1.  Primary Polydipsia 2.  Nutrient poor diet

1.  SIADH 2.  CSW

3.  Hypothyroidism 4.  Secondary Adrenal

Insufficiency

Hypervolemic 1.  CHF 2.  Cirrhosis 3.  Nephro>c

1.  Advanced Renal Failure

Hyponatremia – Correc>on

•  Less than 9mEq/L per 24hr •  Possibly can correct faster IF hyponatremia is less than 48h dura>on (but this is NOT your call)

Hyponatremia -‐ Cases

•  hjp://www.turner-‐white.com/pdf/brm_IM_V10P1.pdf

Hyponatremia -‐ Cases •  62 year old lady presented to the ED with mild dizziness

•  hjps://books.google.com.sg/books?id=fzlOCFYiONUC&pg=PA584&lpg=PA584&dq=hypernatremia+cases&source=bl&ots=RjVBBaMPH7&sig=dOy94vQMhs9ZX6OYaW1d7wmY96Y&hl=en&sa=X&ved=0CF0Q6AEwCTgKahUKEwim0fyt0cHIAhVEJI4KHd2hDi8#v=onepage&q=hypernatremia%20cases&f=false

Tubular Sodium

ADH

Hypernatremia – Pathophysiologic Classifica>on

Too Li9le Water Too Much Sodium

Intracellular Water Shi>

GI Losses Renal Losses

Diabetes Insipidus

OsmoDc Diuresis

Actually ea>ng too much Heavy Exercise

See next slide Hyperglycemic

States

IV Saline overload Seizure

Mannitol

Hypernatremia – Diabetes Insipidus

Central Nephrogenic

Idiopathic (30-‐50%) Renal Disease

Neurosurgery/Trauma Drugs (Esp. Lithium)

Malignancy Hypercalcemia

Infiltra>ve disorders (Eg. Langerhans His>ocytosis)

Hypokalemia

Familial/Congenital Pregnancy

Gene>c Disorders (rare)

Hypernatremia – Clinical Approach

1.  History – PC

•  Diarrhea/Vomit •  Polyuria (Osmo>c Diuresis) •  Altered Mental Status (Beware DKA) •  Seizure

– PmHx •  Debilita>on (Restricted Access)

Hypernatremia – Diagnosing Diabetes Insipidus

1.  Plasma Sodium 2.  Plasma Osmolality + Urine Osmolality – Urine Osmolality <300mOsm/kg = Likely DI

•  Urine < Plasma: Compete DI •  Urine > Plasma: Par>al DI

– Urine Osmolality >600mOsm/kg = Not enough water – Urine Osmolality 300-‐600mOsm/kg = inconclusive

3.  Urine Osmolality response to DDAVP –  <50% increase awer administra>on: Nephrogenic DI –  >50% increase awer administra>on: Central DI

Diabetes Insipidus vs Primary Polydipsia (Presen>ng as Polyuria)

1.  Water Depriva>on test (If presen>ng complaint is polyuria)(to Ddx primary polydipsia) –  Plasma Sodium (abort if >145) –  Plasma Osmolality + Urine Osmolality

•  Urine osmolality >600mOsm/kg = Clearly not DI (more likely primary polydipsia) •  Urine osmolality <600mOsm/kg = Probably DI

–  DDAVP awer WDT •  Urine osmolality >50% increase AND urine corrects to isosmo>c or more concentrated

than plasma = Complete Central DI •  Urine osmolality <50% increase AND urine corrects to isosmo>c or more concentrated

than plasma = Par>al Central DI •  Urine osmolality <50% (usually near 0) increase AND urine corrects to hypotonic to

plasma = Complete Nephrogenic DI •  Urine osmolality >50% increase AND urine corrects to hypotonic to plasma = Par>al

Nephrogenic DI •  Urine osmolality <50% increase AND urine was hypertonic before administering DDAVP =

Primary Polydipsia

Hypernatremia – Cases

•  hjp://highered.mheduca>on.com/sites/0071402357/student_view0/11__kidney__amp__urinary/clinical_case_2.html

Potassium Homeostasis – Renal

Potassium Homeostasis – Cellular

•  Acidosis/Alkalosis – H+ in, K+ out (Electrical neutrality)

•  Insulin/Adrenaline – Cathecholamines + Insulin ac>vate Na/K ATPase to shiw potassium intracellularly

Hypokalemia – Symptoms

•  Muscular generally – Weakness – Arrythmia

Hypokalemia – ECG Changes

•  T wave flajening •  U wave development •  ST depression •  Long PR interval •  If not corrected, Torsade

Hypokalemia – Pathophysiologic classifica>on

Low Input High output Transcellular Shi>

GI Loss Renal Loss

Starva>on Vomi>ng Diure>cs Alkalosis

Anorexia Diarrhea Polyuria Insulin

Laxa>ve abuse Hyperaldosteronism

Cathecholamines

Ureterosigmoidostomy

RTA 1/2 Rapid Cell Prolifera>on

Salt was>ng nephropathy

Hypomagnesemia

Amphotericin B

Hypokalemia – Types of hyperaldosteronism

•  Primary Hyperaldosteronism –  Renin LOW –  Aldosterone HIGH –  Eg. Aldosterone secre>ng tumor/RARE variants of CAH

•  Secondary Hyperaldosteronism –  Renin HIGH –  Aldosterone HIGH –  Eg. Renin secre>ng tumor/Renal artery stenosis

•  Pseudohyperaldosteronism –  Renin and Aldosterone LOW/NORMAL –  Due to other cor>costeroids that have mineralocor>coid aci>vity

–  Eg. Cushings/Exogenous steroids

Hypokalemia – Clinical Approach •  1) History Taking

–  PC •  Diarrhea, Vomiyng •  Diabe>c Crisis (severe polyuria and illness)

–  PmHx •  Cardiac history (diure>cs) •  Severe disability (restricted accessàStarva>on) •  DM •  Asthma (for inhaler use, but rare) •  Blood Cancer Hx (rapidly prolifera>ve)

–  Drug Hx •  Diure>cs •  Insulin use •  Inhaler use (rare)

Hypokalemia – Lab Workup

•  ABG + Urine Potassium •  Serum Renin/Aldosterone Ra>o

Normal/Low Urine Potassium

High urine potassium

Metabolic Acidosis Lower GI Loss RTA 1/2 DKA

Metabolic Alkalosis Upper GI Loss Hyperaldosteronism

Hypokalemia – Treatment

•  ECG + Ajend to pa>ent STAT •  Oral vs IV Potassium – Oral is preferred if possible and potassium is mildly lowered

–  IV is usually used, then swapped to oral later (Burns like crazy, more the faster the infusion runs)

Hyperkalemia – Symptoms

•  Muscular/Cardiac generally – Weakness – Arrythmia

Hyperkalemia – ECG changes

•  String

Hyperkalemia – Pathophysiologic Approach

Input Transcellular Shi> Output

Aldosterone Problems Renal DysfuncDon

IV Drip Cell Breakdown Hypoaldosteronism Acute Kidney Injury

Medica>ons Aldosterone Resistance

Chronic Kidney Disease

Acidosis

Insulin Deficiency

Hyperkalemic Periodic Paralysis

Hyperkalemia – Transcellular Shiws

•  Cell Breakdown 1.  Tumor Lysis Syndrome 2.  Severe hemolysis 3.  Rhabdomyolysis

•  Theore>cally, can be due to heavy exercise •  Medica>ons

1.  Beta blockers (Inhibits Na/K ATPase) 2.  Digoxin Toxicity (Inhibits Na/K ATPase) 3.  Succinylcholine

Hyperkalemia – Aldosterone Problems

•  Hyporeninemic Hypoaldosteronism –  Renal Dysfunc>on (Decreased Renin Produc>on) –  NSAID use

•  Normoreninemic Hypoaldosteronism –  ACE Inhibitors –  Primary Adrenal Insufficiency –  Gene>c Disorders

•  Aldosterone Resistance –  Aldosterone Receptor Blockers –  Bactrim –  Gene>c Disorders

Hyperkalemia – Clinical Approach 1.  ECG + Ajend to pa>ent STAT 2.  Exclude Pseudohyperkalemia (Hemolysed sample)

–  Repeat Bloods 3.  History Taking (Focus on renal func>on and drugs)

–  PC •  Muscle Pain (Rhabdo) •  Trauma (Rhabdo) •  Anemic Symptoms •  Altered Mental Status (Acidosis) •  Hypotension (AKI)

–  PmHx •  Cardiac Hx (Digoxin, other medica>ons) •  Adrenal Insufficiency •  DM (DKA) •  CKD

–  Drug Hx •  Digoxin •  ACE-‐I •  ARBs •  NSAIDs •  Bactrim

4.  Bloods –  Renin, Aldosterone, Cor>sol

Hyperkalemia – Treatment

•  7 Treatments for Hyperkalemia courtesy of Dr Seow CJ 1.  IV Calcium gluconate (stabilise cardiac membrane) 2.  IV Insulin + D50 (Force intracellular shiw) 3.  Resonium (Sodium Polystyrene Sulfonate)(Binds K+

in GI tract) 4.  Inhaled Beta Agonists (Ac>vate Na/K ATPase) 5.  Non-‐potassium sparing diure>cs 6.  Alkalinise blood (please don’t, this is theore>cal) 7.  Hemodialysis

Potassium Case Studies

•  hjps://www.netce.com/casestudies.php?courseid=1199

Approach to Acid-‐Base 1.  Look at pH –  Acido>c or Alkalo>c?

2.  Look at Bicarbonate and PCO2 –  Look for the one deranged in the same direc>on as

the pH 3.  Evaluate compensa>on 4.  Evaluate anion gap for acidosis 5.  Evaluate delta anion gap for complicated

acido>c cases (rarely done) –  For diagnosing triple acid base disorders

Compensa>on Disorder CompensaDon

Metabolic Acidosis PCO2 = 1.5[HCO3-‐] + 8 (+/-‐ 2)

(Winter’s formula)

Metabolic Alkalosis 1 HCO3-‐ increase is 0.7 PCO2 increase

Respiratory Acidosis Acute: 10 PCO2 increase is 1 HCO3-‐

increase

Chronic: 10 PCO2 increase is 4 HCO3-‐

increase

Respiratory Alkalosis Acute: 10 PCO2 decrease is 2 HCO3-‐

decrease

Chronic: 10 PCO2 decrease is 5 HCO3-‐

decrease

Anion Gap and Delta Anion Gap

•  Anion Gap – Posi>ve ions (Na+) – Chief nega>ve ions (HCO3

-‐ and Cl-‐) = 8-‐12

–  Increased gap implies more non-‐calculated anions (usually from dissociated acids)

– Correct for hypoalbuminemia (normal range drops by 2.5 per 1g/dl albumin missing)

•  Delta Anion Gap 𝐶ℎ𝑎𝑛𝑔𝑒 𝑖𝑛 𝑎𝑛𝑖𝑜𝑛 𝑔𝑎𝑝/𝐶ℎ𝑎𝑛𝑔𝑒 𝑖𝑛 𝐵𝑖𝑐𝑎𝑟𝑏𝑜𝑛𝑎𝑡𝑒 

Delta Anion Gap

•  Assumes the bulk of H+ is buffered by HCO3-‐

and thus removes HCO3-‐ from the circula>on

–  In reality, bone buffers a certain amount also •  There should therefore be 1 HCO3

-‐ decrease for every 1 anion gap increase (electrical neutrality)

•  If there is more HCO3-‐ than expected based on

the anion gap, there may be a metabolic alkalosis as well

Osmolal Gap

•  Difference between measured serum osmolality and calculated serum osmolality –  Serum osmolality made up of sodium, chloride, bicarb, urea, glucose

•  Calculated serum osmolality = 2[Na+ in mmol/L] + [glucose in mmol/L] + [urea in mmol/L]

•  A gap of ≥20 suggests weird things in the blood –  Small, osmo>cally ac>ve molecules

•  Usually alcohols of some sort

HAGMA Mnemonics

•  Ketoacidosis •  Uremia •  Lac>c acidosis –  ?Me}ormin

•  Toxins –  Esp. Salicylates

•  Glycols •  Oxoproline •  L-‐lactate •  D-‐lactate •  Methanol •  Aspirin •  Renal failure •  Ketoacids

Ketoacidosis

•  DM (DKA) •  Starva>on •  Chronic Alcoholism (both ketoacidosis and lac>c acidosis) – Ethanol à Acetaldehyde + NADH (NADH s>mulates betahydroxybutyrate produc>on)

– Acetaldehyde à Acetate à Acetyl-‐CoA •  High Acetyl-‐CoA and NADH shunt pyruvate to lactate (Lac>c acidosis)

Uremia

•  Kidney failure à Failure to excrete acids (Anion gap rarely exceeds 20) – NH4

+ –  Phosphate acids – Uric acid – Hippuric Acid –  Sulfates –  Lactate is NOT largely excreted in the urine normally, so will not by itself cause a lac>c acidosis

Lac>c Acidosis •  Cohen-‐Woods Classifica>on –  Type A: Decreased >ssue perfusion –  Type B: No clinical evidence of decreased >ssue perfusion •  B1: Due to underlying disease (eg. Lactate-‐producing cancers)

•  B2: Due to toxins –  Ethanol – Methanol –  Ethylene Glycol (An>freeze, liquid coolants) –  Propylene Glycol (Solvent for some an>epilep>cs) – Medica>ons (eg. HAART)

•  B3: Due to Inborn Error of Metabolism

Other HAGMAs •  Salicylates – Acutely, Metabolic acidosis with Respiratory alkalosis (s>mulates respiratory centre)

– Awer awhile, both Metabolic and Respiratory acidosis (later respiratory suppression)

•  Toluene (glue sniffing) – Metabolised to Hippuric Acid

•  5-‐Oxoproline – Almost Exclusively chronic Acetaminophen use

Clinical Approach to HAGMA 1.  Correct the anion gap 2.  Check ABG to ensure an actual acidosis –  Non-‐acidic nega>vely charged things (paraproteinemia, severe hyperphosphatemia)

3.  Check lactate and ketones –  Lactate high

•  Cohen-‐Woods Type A (Hypoperfusion) –  Systemic hypoperfusion (eg. Shock) –  Regional hypoperfusion (eg. Bowel infarct, limb ischemia)

•  Cohen-‐Woods Type B (No evidence of hypoperfusion) –  Probably toxins/drugs (review drugs, take history of inges>on) –  Lactate producing tumors –  IEMs (should be in medical records these days)

Clinical Approach to HAGMA 3.  Check lactate and ketones –  Ketones high

•  DKA (CBG sky high) •  Alcoholic toxicity (history)

4.  Check renal func>on –  GFR <40 and Anion Gap <20, consider renal failure as diagnosis

5.  Check osmolal gap –  ≥20: Toxic alcohol (Ethanol, Isopropyl Alcohol, Diethyl Ether, Mannitol)

–  <20: Rare diagnoses like 5-‐oxoprolinemia, D-‐lac>c acidosis etc.

NAGMA GI Renal

Gain of H+ Hyperalimenta>on

Type 1 and 4 RTA

Renal Failure

Hyperkalemia

Loss of HCO3-‐

Diarrhea

Type 2 RTA Cholestyramine

Ureteral Diversion

Others: Normal Saline Infusion

Metabolic Alkalosis GI Renal

Loss of H+

Vomi>ng Diure>cs (Except K+ sparing)

NG Suc>on Mineralocor>coid excess

Rare as heck syndromes (Eg. Congenital Chloride

Diarrhea)

Contrac>on alkalosis

Barjer/Gitelman syndrome (rare)

Gain of HCO3-‐

Inges>on of Bicarb Contrac>on alkalosis

Milk-‐alkali syndrome

Respiratory Control of Acid-‐Base

•  O2: Diffusion-‐dependent •  CO2: Ven>la>on dependent •  Ven>la>on control – Central – Neuromuscular – Chest-‐wall compliance

Respiratory Failure

•  Type 1: PO2 low (Diffusion problem) •  Type 2: PO2 low and PCO2 high (Ven>la>on problem)

Respiratory Acidosis -‐ Symptoms

•  CNS symptoms due to hypercapnia and pH changes – Anxiety – Confusion – Somnolence – Delirium – Obtunda>on

Respiratory Acidosis

Lung Problem Central Control Problem

Neuromuscular weakness

Compliance problem

COPD Drugs C3, 4, 5 lesion Kyphoscoliosis

Asthma Brainstem (BEWARE CONING) GBS

Pulmonary Edema Myasthenic Crisis

ILD DMD

Respiratory Alkalosis -‐ Symptoms

•  Hypocalcemic symptoms – Distal parasthesia –  Circumoral parasthesia –  Lightheadedness/Giddiness

•  Acute Central Hypocarbia (cerebral vasoconstric>on) – Dizziness –  Confusion –  Syncope –  Seizure

Respiratory Alkalosis

•  HYPOXEMIA •  Non-‐hypoxic causes – Pain/Anxiety – Drugs

•  Salicylates (early phase) •  Doxapram

– Progesterone (Pregnancy) – Pulmonary edema/embolism, even without hypoxia

electrolytes*and*acid*base* - nigel fong · hyponatremia–pathophysiologic* ... malignancy*...

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electrolytesandacidbase - nigel fong · hyponatremia–pathophysiologic* ... malignancy*...