Surgical Procedures/Acid Base Disorder

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Acid Base Disorder
In general : H+ = 24 × PCO2/HCO3– (Usually in clinical practice, H+ concentration is expressed as pH.)
 * Normal pH = 7.35–7.45.
 * Acidemia = pH < 7.35.
 * Alkalemia = pH > 7.45.
 * PaCO2 (Arterial CO2 concentration normal = 35–45 mm Hg).
 * HCO3– (Serum electrolytes normal = 22–31 mmol/liter).

Acidosis-Alkalosis

 * Acidosis is a process that causes the accumulation of acid.
 * Alkalosis is a process that causes the accumulation of alkali.

Respiratory Acidosis-Alkalosis
Disorders that initially alter arterial PCO2 (arterial CO2 concentration) are termed respiratory acidosis-alkalosis.

Metabolic Acidosis-Alkalosis
Disorders initially affecting HCO3– (serum electrolytes) concentration are termed metabolic acidosis-alkalosis.

Causes

 * 1) Chloride-responsive.
 * 2) *The most common causes in the surgical practice include:
 * 3) **Diuretic therapy (e.g., contraction alkalosis).
 * 4) **Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting).
 * 5) **Exogenous administration of HCO3– or HCO3– precursors (e.g., citrate in blood).
 * 6) Chloride-unresponsive metabolic alkalosis is comparatively less common and includes:
 * 7) *Hyperaldosteronism
 * 8) *Marked hypokalemia
 * 9) *Renal failure
 * 10) *Renal tubular Cl– wasting (Bartter’s syndrome)
 * 11) *Oedematous states.

Diagnosis:
Measurement of urinary chloride concentration.


 * Suggestive causes of the metabolic alkalosis if Urine Cl– concentration is <15 mmol/liter:
 * vomiting.
 * nasogastric suctioning.
 * postdiuretic administration.
 * posthypercapnia.
 * Sughgestive causes of the metabolic alkalosis if Urine Cl– concentration is > 20 mmol/liter:
 * Mineralocorticoid excess.
 * Alkali loading.
 * Concurrent diuretic administration
 * Presence of severe hypokalemia.

Treatment principles in metabolic alkalosis:
Goal of Treatments can be:
 * 1) Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl–, K+, and volume deficits.
 * 2) Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia.
 * 3) H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning.
 * 4) If Edemea:
 * 5) *Acetazolamide (5 mg/kg/day IV or PO) can be used.
 * 6) **Eases fluid mobilization while decreasing renal HCO3– reabsorption.
 * 7) **Tolerance to this diuretic may develop after 2–3 days.
 * 8) Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3– >40 mmol/liter; rate not exceeding 5 ml/minute).
 * 9) *Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl– concentration is usually rechecked to determine the need of further treatment.
 * 10) *Hepatic failure is contraindication for NH4Cl.
 * 11) HCl more rapidly corrects metabolic alkalosis.
 * 12) Dialysis:
 * 13) *Can be considered in the volume-overloaded situation with renal failure and intractable metabolic alkalosis.

Estimation of the amount of H+ requirement
The amount of H+ to administer may be estimated by the following equation: H+(mmol) = 0.5 × wt (kg) × [103 – serum Cl– (mmol/liter)]

Estimation of the amount of NH4Cl requirement:
Can be estimated by the following equation: NH4Cl (mmol) = 0.2 × wt (kg) × [103 – serum Cl– (mmol/liter)]

Metabolic Acidosis
(Low pH with low CO2 content)
 * Reduction in plasma Bicarbonate and a consequence rise in H+.
 * PaCO2 is reduced secondarily by Hyperventilation, which mitigates the rise in H+.

Causes
Metabolic Acidosis is caused if:
 * Accumulation of nonvolatile acids.
 * Reduction of renal acid excretion.
 * Loss of alkali.

Mnemonics
MUD PILES

1.	Methyl Alcohol. 2.	Uremia. 3.	Diabetic Ketoacidosis 4.	Para-Aldehyde poisoning. 5.	Ischemia. 6.	Lactic acidosis. 7.	Ethylene Glycol Alcohol ingestion. 8.	Salicylic Poisoning.

Other commonest causes are:

 * Addition of excessive acids to plasma.
 * Ketoacidosis, Lacticacidosis.
 * Methanol, ethylene glycol and salicylic poisoning.
 * Failure to excrete acid:
 * Chronic Renal Failure.
 * Acute Renal Failure etc
 * Loss of Bicarbonate (base):
 * From G.I.T:
 * Diarrhea.
 * Fistulae.
 * In Urine:
 * Proximal renal tubular acidosis.
 * Carbonic anhydrase inhibitors.

Clinical Feature

 * 1) Usually in severe cases Kussmaul's respiration can be present.
 * 2) When H+ >70 mmol/L; then,
 * 3) *Cardiac-Out-Put falls.
 * 4) *Blood pressure decreases.
 * 5) *Frequnet confusion.
 * 6) *Drowsiness.

Diagnostic Classsification (Anion Gap)
Anion gap (AG: normal, 3–11 mmol/liter) AG (mmol/liter) = Na+ (mmol/liter) – [Cl– (mmol/liter) + HCO3– (mmol/liter)]

It is useful diagnostically to classify metabolic acidosis into:


 * 1) Increased AG metabolic acidosis.
 * 2) Normal AG metabolic acidosis.

Increased anion gap Metabolic Acidosis:

 * 1) Increased acid production:
 * 2) Ketoacidosis
 * 3) Diabetic
 * 4) Alcoholic
 * 5) Starvation
 * 6) Lactic acidosis
 * 7) Toxic ingestion:
 * 8) Salicylates.
 * 9) Ethylene glycol.
 * 10) Methanol.
 * 11) Renal failure.

Normal anion gap (hyperchloremic) Metabolic Acidosis:

 * 1) Renal tubular dysfunction
 * 2) Renal tubular acidosis.
 * 3) Hypoaldosteronism.
 * 4) Potassium-sparing diuretics.
 * 5) Loss of alkali.
 * 6) Diarrhea.
 * 7) Ureterosigmoidostomy.
 * 8) Carbonic anhydrase inhibitors.
 * 9) Administration of HCl (ammonium chloride, cationic amino acids).

Management/Treatment of metabolic acidosis:

 * Directed primarily towards the underlying cause of the acid-base disturbance.
 * Bicarbonate therapy is considered when there is moderate to severe metabolic acidosis, depending on the etiology.

The HCO3– deficit (mmol/liter) can be estimated by the following equation:
 * 1) Infusion of NaHCO3, stoped when H+ is normol.
 * 2) Monitoring H+ and HCO3-
 * 3) Treatment of underlying causes.

HCO3– deficit (mmol/liter) = Body weight (kg) × 0.4 × [desired HCO3– (mmol/liter) – measured HCO3– (mmol/liter)]

(This equation serves only as a rough estimate .)

The goal of HCO3–

 * To raise the arterial blood pH to 7.00 or the HDRO3– concentration to 10 mmol/liter.
 * Risks of bicarbonate therapy:
 * Hypernatremia.
 * Hypercapnia.
 * Cerebrospinal fluid acidosis.
 * Overshoot alkalosis.

Serial arterial blood gases and serum electrolytes should be obtained to assess the response to HCO3– therapy.

Rate of HCO3– replacement:

 * In nonurgent situations:
 * Continuous intravenous infusion over 4–8 hours (50-ml ampule of 8.4% NaHCO3 solution provides 50 mmol of HCO3–) can be added to 1 liter of D5W or 0.45% NaCl.
 * In urgent situation:
 * Deficit can be administered as a bolus over several minutes.