For study and discussion

1. Genital Trauma
Presenter:
Dr.Muhammad Husnain

2. Metabolic Acidosis
Presenter:
Dr.M.Husnain

3. Definition of Metabolic Acidosis
• Acidosis : is a process that increases [H+]
• Acidemia: When blood pH <7.35
• Metabolic acidosis: When an acid other than carbonic acid
accumulates in the body resulting fall in HCO3- concentration.
• Mechanism:
• gain of H+
• loss of HCO3-
• Results in:
• ↓pH (7.35)
• ↓HCO3- (<22mEq/L)
• pCO2 depends on compensation

5. Urinary Anion Gap:
UAG=(UNa+UK)-UCl
• The UAG is normally a positive value, ranging from +30 to +50
mmol/l.
• A negative value for the UAG suggests increased renal excretion of an
unmeasured cation (i.e., cation other than Na+ or K+) one such cation
is NH4+.
• With chronic metabolic acidosis because of extrarenal causes, urinary
ammonia concentrations, in the form of NH4Cl, can reach 200 to 300
mmol/l.
• As a result, the measured cation concentration will be less than the
measured anion concentration, which includes the increased urinary
Cl−, and the UAG will be less than zero and frequently less than −20
mmol/l.

6. Anion Gap:
• ([Na+] + [K+]) − ([Cl-] + [HCO3−])
• Anion gap (AG) = [Na+] − ([Cl-] + [HCO3−])
• Unmeasured anions subtracted by unmeasured cations (in ECF)
• Omission of potassium has become widely accepted, as potassium
concentrations, being very low, usually have little effect on the
calculated gap.
• Normal value: 12mmol/L(+_2)

7. • ↑AG = ↑ unmeasured anions such as organic acids, phosphates,
sulfates
• ↓AG = ↓ alb or ↑ unmeasured cations (Ca,Mg, K, Li, bromine,
immunoglobulin)

8. Low Anion Gap:
• A low anion gap is frequently caused by hypo albuminemia.
• In hypo albuminaemia the anion gap is decreased by 2.5 per 1 g/dL
decrease in serum albumin.
• The anion gap is sometimes reduced in multiple myeloma, where
there is an increase in plasma IgG (para proteinaemia).
• expected AG is [albumin] X2.5 (i.e, 10 if albumin is 4 g/dL)

9. Causes:
• Renal Tubular Acidosis
• Gastrointestinal Base Loss(loss of HC03-)
• Inorganic acid poisoning(addn of anions)
• Ureteral diversion
• Ketoacidosis: Diabetic, Starvation
• Lactic Acidosis
• Renal Failure
• Poisoning: Ethanol Glycol, Methanol, Aspirin,Acetaminophen

10. • Lactic Acidosis
• Type A: impairment in tissue oxygenation examples are circulatory or
respiratory failure, sepsis, ischemic bowel, carbon monoxide, cyanide
• Type B: no impairment in tissue oxygenation examples are
malignancy, alcoholism, meds (metformin , NRTIs, salicylates,
propylene glycol)

12. • Methanol (windshield fluid, antifreeze, solvents, fuel): metabolise to
formic acid
• Ethylene glycol (antifreeze): metabolise to glycolic and oxalic acids
• Propylene glycol (pharmaceutical solvent, eg, IV diazepam &
lorazepam antifreeze): lactic acidosis
• Salicylates: metabolic acidosis (from lactate,ketones) respiratory
alkalosis due to stimulation CNS respiratory center
• Acetaminophen: glutathione depletion -> increase endogenous
organic acid 5-oxoproline in susceptible host (malnourished, female,
renal failure)

16. Consequence of Acidemia on various
Organ System:

17. Investigation
• Evaluate history for causes(diarrhea, ingestion of mineral acids/drugs,
kidney diseases,diabetes, any diversional surgery, starvation)
• For suspected ketonuria (dipstick acetoacetate) or plasma
hydroxybutyrate [as urine aceto-acetate often not present in early
ketoacidosis due to shunting to ᵝOH butyrate,aceto-acetate may later
turn +ve]

18. If Ketones negative
• renal function, lactate(inc by about 10 fold in lactic acidosis), toxin
screen, and osmolal gap
• Osmolal gap (OG)=measured osmoles -calculated Osmoles
• calculated osmoles
(2 XNa)+(glucose/18)+(BUN/2.8)
• OG>10 suggests ingestion

19. • In case of hyper chloraemic (normal anion gap) acidosis with no
evidence of gastrointestinal disturbance and Urine pH is
inappropriately high>5.5 in presence of systemic acidosis points toward
Renal Tubular Acidosis.

21. Proximal RTA (Type 2)
• ↓ proximal re-absorption of HCO3
• E.g: Fanconi Syndrome, Multiple Myeloma,Amyloidosis, Myeloma,
Carbonic Anhydrase inhibitor
• Urinary pH <5.3, moderate acidosis, serum K+ normal or low

24. Classical Distal RTA (Type 1)
• defective distal H+ secretion
• E.g.: Congenital, Autoimmune(RA, Sjogren’s),SLE, Drugs (Lithium,
Amphotericin)
• pH of a fresh sample of urine is > 5.5. Serum potassium level is
normal or low. Urine anion gap is positive because of inadequate
hydrogen ion secretion

26. Hyperkalaemic distal RTA (type 4)
• Hypo aldosteronism
• Obstructive Nephropathy
• Drugs: Amiloride, Spironolactone, ACEI, ARB,NSAIDs
• Diseases: Sickle cell, SLE, Amyloidosis
• urine pH is < 5.5. Serum potassium level is elevated. Urine anion gap
is positive because of defective NH3 generation.

30. Compensation
• Early compensation by respiratory system by hyperventilation washes
out Co2 to restore the pH level
• Late compensation is by kidneys which causes excretion of H+ and
retention of HCO3-

32. Management:
• Initially resuscitation with IV fluids is often needed.
• DKA: insulin & IVF; dextrose, IVF, replete K,Mg, PO4 as needed
• Lactic acidosis: treat underlying condition, avoid vasoconstrictors
• Renal failure: hemodialysis
• Methanol & ethylene glycol: early fomepizole, vit. B6 (ethylene
glycol), folate(methanol),hemodialysis (especially if late presentation)
• Alkali therapy: NaHCO3

33. • Use of IV bicarbonate is controversial
• Rapid correction causes hypokalemia or reduced plasma ionised
calcium
• To be used in critical acidosis (pH <7.00)
• In RTA type 1 & 2 supplements of Na & K bicarbonate are necessary
• In RTA type 4 diuretics of loop or thiazide class may be effective in
increasing acid secretion.