# 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.

#### Metabolic Alkalosis
##### Causes

* Chloride-responsive.
** The most common causes in the surgical practice include:
*** Diuretic therapy (e.g., contraction alkalosis).
*** Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting).
*** Exogenous administration of HCO3– or HCO3– precursors (e.g., citrate in blood).
* Chloride-unresponsive metabolic alkalosis is comparatively less common and includes:
** Hyperaldosteronism
** Marked hypokalemia
** Renal failure
** Renal tubular Cl– wasting (Bartter’s syndrome)
** 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:
* Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl–, K+, and volume deficits.
* Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia.
* H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning.
* If Edemea:
** Acetazolamide (5 mg/kg/day IV or PO) can be used.
*** Eases fluid mobilization while decreasing renal HCO3– reabsorption.
*** Tolerance to this diuretic may develop after 2–3 days.
* Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3– >40 mmol/liter; rate not exceeding 5 ml/minute).
** 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.
** Hepatic failure is contraindication for NH4Cl.
* HCl more rapidly corrects metabolic alkalosis.
* Dialysis:
** 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

* Usually in severe cases Kussmaul's respiration can be present.
* When H+ >70 mmol/L; then,
** Cardiac-Out-Put falls.
** Blood pressure decreases.
** Frequnet confusion.
** 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:
* Increased AG metabolic acidosis.
* Normal AG metabolic acidosis.

##### Causes according to Anion Gap:
###### Increased anion gap Metabolic Acidosis:

* Increased acid production:
** Ketoacidosis
*** Diabetic
*** Alcoholic
*** Starvation
** Lactic acidosis
** Toxic ingestion:
*** Salicylates.
*** Ethylene glycol.
*** Methanol.
* Renal failure.

###### Normal anion gap (hyperchloremic) Metabolic Acidosis:

* Renal tubular dysfunction
** Renal tubular acidosis.
** Hypoaldosteronism.
** Potassium-sparing diuretics.
* Loss of alkali.
** Diarrhea.
** Ureterosigmoidostomy.
** Carbonic anhydrase inhibitors.
* 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.
* Infusion of NaHCO3, stopped when H+ is normal.
* Monitoring H+ and HCO3-
* Treatment of underlying causes.
The HCO3– deficit (mmol/liter) can be estimated by the following equation:
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.