View source for Acid-Base Disorders (Neonatology)

Normal values of [[Acid-base balance|acid-base balance (ABR)]] or ''examination of blood gases and internal environment according to Astrup'' depend on the sampling site (arterial/venous/capillary) and the gestational age of the newborn.
The measured values include pH, pCO<sub>2</sub> and O<sub>2</sub>, other values are added (excess/deficiency of bases, bicarbonate, oxygen saturation).

The gold standard is [[Laboratory examination of acid-base balance|ABR examination]] from arterial blood (from a peripheral arterial catheter or an umbilical arterial catheter). Venous ABR has lower pH, higher pCO<sub>2</sub> and low/not evaluable pO<sub>2</sub> compared to arterial blood. Capillary ABR (from heated heel) has pH and pCO<sub>2</sub> values closer to arterial blood than venous sample (values the same or slightly different), pO<sub>2</sub> is low/not evaluable. Normal arterial pH is 7.30-7.40 and normal capillary pH is 7.25-7.35. It is not possible to draw conclusions from a single ABR examination, the development of ABR over time and the context (clinical condition, etc.) are important.<ref name="Gomella2020">{{Cite | type = book | surname1 = Gomella | name1 = Tricia | surname2 = Eyal | name2 = Fabien | surname3 = Bany-Mohammed | name3 = Fayez | title = Gomella's Neonatology | edition = 8 | publisher = McGraw-Hill Education | year = 2020 | isbn = 9781259644818 | range = 1472 | pages = 98, 431-442}}</ref>

{| class="wikitable"
  ! colspan="8" | Normal arterial blood ABR values of newborns (at normal body temperature and normal hemoglobin)<ref name="Gomella2020"/>
  |-
  ! rowspan="2" | Gestational age !! rowspan="2" | pH !! colspan="2" | p<sub>a</sub>O<sub>2</sub> !! colspan="2" | p<sub>a</sub>CO<sub>2</sub> !! rowspan="2" | HCO<sub>3</sub> <br/> (mmol/l) !! rowspan="2" | BE/BD
  |-
  ! (mm Hg) !! (kPa) !! (mm Hg) !! (kPa)
  |-
  ! A full-term newborn
  | 7.32-7.38 || 80-95 || 10.7-12.7 || 35-45 || 4.7-6.0|| 24-26 || ± 3.0
  |-
  ! 30-36 week of gestation
  | 7.30-7.35 || 60-80 || 8.0-10.7 || 35-45 || 4.7-6.0 || 22-25 || ± 3.0
  |-
  ! < 30th week of gestation
  | 7.27-7.32 || 45-60 || 6.0-8.0 || 38-50 || 5.0-6.7 || 19-22 || ± 4.0
|}
BE/BD = base excess/deficiency; body temperature 37 °C; hemoglobin 148-155 mg/l.

====Anion gap====
* the difference between measured cations and anions in serum or plasma:

<div class="example">
Anion gap (mmol/l) = Na (mmol/l) - [Cl (mmol/l) + HCO<sub>3</sub> (mmol/l)]
</div>

* normal values: 8-16 mmol/l (up to 18 mmol/l in premature newborns < 1000 g).<ref name="Gomella2020"/>

==Differential diagnosis==
===Metabolic acidosis (MAC)===
* ↓ pH and ↓ HCO<sub>3</sub> (normal/low pCO<sub>2</sub>).
* Main causes: loss of bases (bicarbonate) from renal or gastrointestinal causes, reduced renal acid excretion or increased acid production.
* occurs in severely ill newborns;
* mild metabolic acidosis is common shortly after birth.

* '''MAC + increased anion gap'''' (> 16 mmol/l; in newborns < 1000 g: > 18 mmol/l); normal chlorides ⇒ another acid is additionally present:
** '''Lactic acidosis''''
*** causes: [[Asphyxia of the newborn|asphyxia]], hypoxia, [[Respiratory distress syndrome (pediatrics)|respiratory distress syndrome]], [[Sepsis (neonatology)|sepsis]], [[Heart failure (neonatology)| impaired cardiac output]] (cardiogenic, septic and hypovolemic shock), circulatory or ventilatory failure, massive bleeding, severe [[Anemia in the neonatal period|anemia]], intracranial bleeding, hypothermia, hypotension, [[Open Botall's duct|PDA]] , [[necrotizing enterocolitis]], intestinal ischemia, excessive ventilation pressures compromising cardiac output, [[Neonatal convulsions|convulsions]], ascites, leakage of fluids into the third space.
** '''Inborn metabolic defects''' (lactic acidosis without signs of impaired tissue perfusion)
*** causes: [[organic acidemia]] (most common), [[galactosemia]], [[hereditary fructose intolerance]], [[maple syrup disease]], congenital/primary lactic acidosis, [[Glycogenoses|glycogenosis type I ]], [[Mitochondrial disease|pyruvate dehydrogenase/carboxylase deficiency]], [[Mitochondrial disease|defects of the mitochondrial respiratory chain]], [[Mitochondrial disease|fatty acid oxidation disorders]] (persistent MAC, increased anion gap, negative ketones in urine, [[HELLP syndrome]] mother).
** '''Acute kidney damage, chronic kidney disease''' (failure to excrete hydrogen ions and other acidic anions)
** '''Late metabolic acidosis of immaturity''' (1st to 3rd week of life, impaired growth; with excess protein intake)
** '''Toxins and drugs''': maternal use of salicylates, maternal acidosis; alcohols and glycols, acetaminophen, α-adrenergic agent, cocaine, ibuprofen, iron, valproate,...
* '''MAC + hyperchloremia'''; normal anion gap
** Most common causes: renal tubular acidosis and diarrhea. Low potassium ⇒ loss of bases. High potassium ⇒ renal tubular acidosis.
** '''Renal bicarbonate losses''': immature kidneys, renal tubular acidosis (impairment of bicarbonate reabsorption or hydrogen ion secretion), acute kidney injury, renal dysplasia, drugs (spironolactone, etc.), hypoaldosteronism (↓ Na<sup>+ </sup> and ↑ K<sup>+</sup>), [[Hyperparathyroidism|hyperparathyroidism]].
** '''Gastrointestinal bicarbonate losses'''': diarrhea (secretory), urological and GIT procedures (surgical intervention in [[Necrotizing enterocolitis|NEC]], ileostomy, enterocutaneous or intestinal fistula, drainage of the small intestine or pancreas..), drugs (cholestyramine, CaCl<sub>2</sub>, MgSO<sub>4</sub>,...).
** '''Dilution acidosis''' - rapid volume expansion with solutions of ringer lactate, physiological solution, glucose with dilution of bicarbonates.
** '''Excess chlorides in IV fluids'''.
** False acidosis - with excess heparin in the syringe, with air admixture in the sample.
** Hyperalimentation acidosis.
** [[Potassium-sparing diuretics]] and hyperkalemia.<ref name="Gomella2020"/>

===Metabolic alkalosis===
* ↑ pH and ↑ HCO<sub>3</sub> (pH > 7.45 and BE > 5).
* Infrequent in newborns, usually iatrogenic with excessive supply of HCO<sub>3</sub> (e.g. chronic alkalinization) or with excessive losses of H<sup>+</sup> (e.g. with losses of gastric juices or diuretic therapy) .

* '''MAL chloride-resistant''' (high chloride content in urine, > 20 mmol/l); increased volume of extracellular fluids:
** causes: excessive administration of alkaline solutions (acetate, bicarbonate, malate), early diuretic therapy (furosemide), hypokalemia, transfusion of a large volume of blood derivatives, [[Bartter's syndrome]] (administration of [[Mineralocorticoids|mineralocorticoids]]), exogenous administration [[Corticosteroids (signpost)|steroids]], [[Cushing's syndrome|Cushing's]], [[Conn's syndrome|Conn's]] or [[Liddle's syndrome]], [[primary aldosteronism]], variants of congenital adrenal hyperplasia (excess syndrome deoxycorticosterone), [[milk-alkali syndrome]] (excess calcium and alkali intake), neonatal pseudo-Barterra syndrome (secondary to maternal eating disorders);
* '''MAL chloride-responsive''' (low urinary chloride content, < 10 mmol/l); low serum chloride level, reduced extracellular fluid volume:
** losses of gastric fluid (persistent vomiting, continuous suction from the stomach), secretory diarrhea (congenital chloride-wasting diarrhea), acute correction of chronic compensated respiratory acidosis, late diuretic therapy, post hypercapnic syndrome;
* '''common causes of MAL in newborns''':
** prolonged suction from the stomach (naso/orogastric tube);
** diuretic therapy (furosemide in children with [[Bronchopulmonary dysplasia|BPD]]);
** excessive administration of bases (sodium bicarbonate, citrate, acetate, lactate) in parenteral nutrition or increased enteral supply of bases
** potassium deficiency;
** compensation of respiratory acidosis (children with BPD/CLD, chronic ventilation).<ref name="Gomella2020"/>

===Respiratory acidosis===
* ↓ pH and ↑ pCO<sub>2</sub> (insufficient alveolar ventilation → ↑ pCO<sub>2</sub>).
* In children with BPD, a higher pCO<sub>2</sub> level is sometimes tolerated, so-called permissive hypercapnia.
* Main causes:
** obstruction of the endotracheal tube (e.g. mucus);
** wrong position of the endotracheal cannula (end in the oropharynx, or vice versa in the right bronchus or on the carina);
** insufficient ventilation support or ventilator failure (circuit disconnection, etc.);
** progression of respiratory failure ([[Respiratory distress syndrome (pediatrics)|RDS]], [[transient tachypnea of the newborn]], pneumonia, [[Bronchopulmonary dysplasia|BPD/CLD]], [[pleural effusion]], [[atelectasis ]],...);
** pneumothorax;
** hypoventilation, insufficient respiratory effort (effect of maternal anesthesia, medication, [[neuromuscular disorders]], congenital central hypoventilation syndrome, [[Sepsis (neonatology)|sepsis]], intracranial hemorrhage, [[Hypoglycemia of the newborn|hypoglycemia]]);
** [[open duct of Botall]] (PDA) with pulmonary edema;
** pulmonary hypoplasia, [[Congenital diaphragmatic hernia|congenital diaphragmatic hernia]], paralysis of the phrenic nerve etc.<ref name="Gomella2020"/>

===Respiratory alkalosis===
* ↑ pH and ↓ pCO<sub>2</sub>.
* CAVE: may be accompanied by reduced cerebral blood flow and reduced tissue oxygen supply (→ hypocapnia is associated with [[Periventricular leukomalacia|periventricular leukomalacia]] and deafness).
* Main causes:
** "overventilation" [[Artificial pulmonary ventilation (neonatology)|pulmonary ventilator]];
** air bubble in the analyzed blood sample;
** heparin in the analyzed blood sample (heparin falsely reduces pCO<sub>2</sub>);
** central hyperventilation (increased respiratory drive, e.g. in case of CNS damage or transient hyperammonemia);
** hypoxemia (hypoxemia stimulates the respiratory center through chemoreceptors → hyperventilation);
** hyperventilation during [[Sepsis (neonatology)|sepsis]], fever, aspiration pneumonia, etc.
** compensation of metabolic acidosis.<ref name="Gomella2020"/>

==Notes on ABR correction==
Do the ABR values correspond to the development of the clinical condition? If not, repeat the examination. (CAVE: bubble or heparin in the analyzed sample → false RAL)

===MAC Correction===
* diagnosis and treatment of the cause (eg, hypoxia, hypovolemia, sepsis, bleeding, low cardiac output, severe anemia);
* MAC is not corrected by hyperventilation (↓ pCO<sub>2</sub> ⇒ ↓ cerebral blood flow ⇒ risk of [[periventricular leukomalacia]]);
* volume expansion is given only for signs of hypovolemia (severe MAC ⇒ reduced myocardial contractility);
* correction of MAC by administration of bicarbonate is controversial (NaHCO<sub>3</sub> ⇒ ↑ natremia, transient fluctuations of cerebral blood flow, risk of intracranial bleeding, worsening of cardiac functions, reduced tissue oxygen supply, progression of intracellular acidosis); the administration of NaHCO<sub>3</sub> can be considered in the substitution of chronic GIT/kidney losses, in the urgent treatment of severe hyperkalemia accompanied by changes on the ECG, acute decompensation of some congenital metabolic defects, or severe, life-threatening metabolic acidosis;
** 8.4% solution of NaHCO<sub>3</sub> (sodium bicarbonate) is a one-molar solution - this means that there is 1 mmol of NaHCO<sub>3</sub> in 1 ml of solution;
** NaHCO<sub>3</sub> is a hypertonic solution (⇒ dilute sufficiently with Aqua for injection, administer into a large vein; max. IV concentration 0.5 mmol/ml = max. 4.2% NaHCO<sub> 3</sub>);
** "half" correction according to ABR: HCO<sub>3</sub><sup>-</sup> (mmol) = 0.3 × base deficit (mmol/l) × weight (kg) × 0.5
** give slowly i.v. (max. 1 mmol/kg/h); ensure adequate CO<sub>2</sub> ventilation (NaHCO<sub>3</sub> → H<sub>2</sub>CO<sub>3</sub> → CO<sub>2</sub > and H<sub>2</sub>O);
* correction of MAC by administration of sodium acetate (or sodium ethanoate or sodium acetate; CH3COONa = organic acid salt; after metabolizing organic anions, a strong cation remains in excess and bicarbonate is generated to maintain electroneutrality and its concentration in the blood increases);
** dosage same as bicarbonate;
* during MAC correction, it is necessary to monitor potassium (↑ pH ⇒ ↓ potassium ⇒ risk of hypokalemia);
* in persistent MAC, congenital metabolic defects must be ruled out.<ref name="Gomella2020"/>

{{Working}}
<noinclude>== References ==

=== Related Articles ===
* [[Acid-base balance]]
* [[Laboratory examination of acid-base balance]]
* [[Relationships between acid-base balance and ionogram]]
* [[Acid-base_balance disorders]]
* [[Combined disorders_of_acid_base_balance]]
* [[Correction and compensation of acid-base balance disorders]]
* [[Principles of treatment_of_acid-base_balance_disorders]]
=== External links ===
=== References ===
<references />
</noinclude>
[[Category: Neonatology]]
[[Category: Paediatrics]]