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HOW TO ... Approach For Metabolic acidosis

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Tawaa Al-salman

on 28 October 2013

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Transcript of HOW TO ... Approach For Metabolic acidosis

HOW TO ... Approach For Metabolic Acidosis ???

Definition :
simple metabolic acidosis
is an acid-base disorder characterized by an
arterial pH of less
than
7.35
in
the
absence
of an
elevated PaCO2
. It is created by 1 of 3 mechanisms:
(1)
Loss
of
bicarbonate
from the body.

(2) Impaired ability to
excrete

acid
by the kidney.

(3)
Addition
of
acid
to the body.



Causes of metabolic acidosis
HOW to find the cause ?!
Solution
The Result ...
What dose our body response ??!!
it has to compensate the problem

HOW

Respiratory compensation
kidney compensation
kidney
start
to
excrete an increased

acid load

12-24 hours
after the compensatory hyperventilation begins and continues for
1-3 days
.
Over time
, the kidneys attempt to
increase reabsorption
of
HCO3
- to compensate for the acidosis.
medullary chemoreceptors
compensate for a metabolic acidosis through
increases in alveolar ventilation.
The resulting
tachypnea and hyperpnea to
reduces the PaCO2 process happens
quickly
and is complete within
12-24 hr.


Note
:
appropriate respiratory compensation for a metabolic acidosis
never
normalizes the patient's pH.

Anion gap !
No. of -
ve
charged ions (
anions
) should
equal
the No. of +
ve
charged ions (
cations
) to give
zero
net charge .
Measured serum
anions
are
Cl and Hco3
, and the
unmeasured anions include phosphates, So4, and proteins (eg, albumin).
The measured serum
cation
is
Na,
but other cations are noted,
such as Ca, K, and Mg.
Anion Gap = (Sodium) – (Chloride + Bicarbonate)

Normally
(8-12mEq/L)
Metabolic Acidosis is divided into processes that are associated with
Normal anion gap (8-12 mEq/L)
Diagnosis
History :
h\o
diarrhea
h\o
seizures, a depressed sensorium, or both in a neonate - This warrants consideration of an inborn error of metabolism, or neonatal sepsis .
h\o
depressed mental status, lethargy, and poor feeding in a neonate - Left-sided, obstructive cardiac lesions should be considered (eg, aortic coarctation or hypoplastic left heart syndrome)
Physical examination
*Hyperventilation or Kussmaul breathing.

*impaired cardiac contractility ,arrhythmia , hypotension.

*Signs of dehydration may include tachycardia, dry mucous membranes, and delayed capillary refill.

*Patients with diabetic ketacidosis may present with fruity odor to their breath

*Hepatomegaly and metabolic acidosis may occur in children with sepsis, congenital or acquired heart disease, hepatic failure, or inborn errors of metabolism.


*neurologic signs that may indicate meningitis or
inborn error of metabolism



Investigation
*
h\o
Failure to thrive suggestive of chronic metabolic acidosis in RTA,
*h\o
New onset of polyuria, polydipsia, and weight loss -DM DKA
*
h\o
ingestion of a toxin or medications .
*
h\o
trauma, or fever
*
h\o
states associated with a lactic acidosis secondary to shock from hypovolemia, sepsis, cardiac failure, anaphylaxis, or spinal shock

normoglycemia, and glycosuria occur in children when type II RTA is part of Fanconi syndrome;
An
increased
anion gap occurs when there is an
increase
in
unmeasured anions.
Common diseases
Diarrhea
Normal AG

most common cause ....

low >>> Hco3 ,Na ,H2O,K
increase >>>> lactic acid , aldosterone,


DKA
hyperglycemia .
ketonemia or ketonurea
low Hco3
high anion gap

RTA
In distal RTA
hypokalemia
,
hypercalciuria
,
nephrolithiasis
, and
nephrocalcinosis
.
Patients with distal RTA cannot acidify their urine and, thus, have a urine
pH >5.5
despite a metabolic acidosis.

Failure to thrive due to chronic metabolic acidosis is the most common presenting complaint.


Proximal RTA

glycosuria
,
aminoaciduria
, and excessive
urinary losses of phosphate and uric acid
pH <5.5
.
Note : bicarbonate therapy increases bicarbonate losses in the urine, and the urine pH increases.


Rickets and/or failure to thrive may be the presenting complaint


hyperkalemic RTA

due to either an
absence of aldosteron
e or an inability of the kidney to
respond to aldosterone

hyperkalemia
and metabolic acidosis are accompanied by
hyponatremia
This is done by :
Dr.Tawaa Nasser Al-Salman
NORMAL VALUES OF ARTERIAL BLOOD GASES
pH 7.35-7.45
[HCO3−] 20-28 mEq/L
Pco2 35-45 mm Hg


the Henderson-Hasselbalch equation, emphasizes the
relationship
among
the
Pco2
, the
bicarbonate
concentration, and the
hydrogen
ion concentration:





An
increase
in the
Pco2
or a
decrease
in the
bicarbonate
concentration
increases
the hydrogen ion concentration; the pH
decreases
.

A
decrease
in the
Pco2
or an
increase
in the
bicarbonate
concentration
decreases
the hydrogen ion concentration; the pH
increases
.


Facts
Acidemia
is a
pH below normal (<7.35)
An
acidosis
is a pathologic process that causes an
increase in the hydrogen ion concentration.
Whereas acidemia is always acidosis


BUT

a patient can have an acidosis and a low, normal, or high pH.

EX , a patient may have a mild metabolic acidosis but a simultaneous, severe respiratory alkalosis; the net result may be alkalemia.
SO
,
Acidemia and alkalemia indicate the pH abnormality; acidosis and alkalosis indicate the pathologic process that is taking place


Metabolic Acidosis either :
simple

mixed

GI bicarb loss
Diarrhea
Ureteral diversion

Impaired renal acid excretion
renal failure
classic distal RTA (type I)
hyperkalemic distal RTA (type IV)

Renal bicarbonate loss
proximal RTA (type II)
carbonic anhydrase inhibitors

Posthypocapneic state
HCl administration






elevated anion gap (>12 mEq/L).
lactic acidosis:
Poisoning:
Ethylene glycol

Methanol

Salicylate

Toluene

Paraldehyde



Ketoacidosis:

Diabetic ketoacidosis

Starvation ketoacidosis

Alcoholic ketoacidosis

kidney failure
Others

Liver failure

Malignancy

Intestinal bacterial overgrowth

Inborn errors of metabolism
Tissue hypoxia: Shock Hypoxemia Severe anemia

Medication

Nucleoside reverse transcriptase inhibitors

Metformin

Propofol
measurements of electrolytes, BUN, creatinine, and serum glucose levels.
urine analysis .

Calculate the anion gap from the electrolyte levels. This guides the initial diagnostic approach (ie, for a normal or elevated anion gap).


Brine storming
Patients have elevated BUN and CR suggesting rena lBUN-to-creatinine ratio greater than 20:1 supports the diagnosis of prerenal azotemia and hypovolemia.

Hypoglycemia associated with a metabolic acidosis can be caused by adrenal insufficiency or liver failure.


Hyperglycemia, glycosuria, ketonuria, and a metabolic acidosis support the diagnosis of diabetic ketoacidosis.

potassium
The combination of metabolic acidosis, hyperkalemia, and hyponatremia occurs in patients with severe aldosterone deficiency (adrenogenital syndrome) or aldosterone resistance.
T
he serum potassium level is often abnormal

metabolic acidosis causes K to move from the intracellular space to the extracellular space,

a
low serum K leve
l owing to excessive body losses of K.
diarrhea, in type I or type II RTA,

. In
DKA
, urinary losses of K are high, but the shift of potassium out of cells due to lack of insulin and metabolic acidosis is significant.
total body K is almost always decreased.

a serum
K level is increased
with acidosis due to
renal insufficiency; urinary potassium excretion is impaired.

Hyperchloremic metabolic acidosis
Inborn error of metabolism
normal AG
A mixed acid-base disorder is present when there is
more than 1 primary
acid-base disturbance.
pneumonia
and
sepsis
may have severe acidemia due to a combined metabolic acidosis caused by lactic acid and respiratory acidosis caused by ventilatory failure.
A patient has a primary metabolic acidosis with a serum bicarbonate concentration of 10m Eq/L. The expected respiratory compensation is a carbon dioxide concentration is ???
(1.5 x 10 + 8 +\- 2 =
23 mmhg
Calculate the excess anion gap (total anion gap minus 12) and add this value to the measured bicarbonate concentration; if the sum is greater than 30 mmol/L there is an underlying metabolic alkalosis; if the sum is less than 23 mmol/L there is an underlying non-anion gap metabolic acidosis.

Blood gas: 7.40 / 40 / 24
Na= 145, Cl= 100
pH normal
AG = 21 (primary metabolic acidosis)

Metabolic Acidosis and Metabolic Alkalosis
This patient had chronic renal failure (met. acidosis) and began vomiting (met. alkalosis) as his uremia worsened. The acute alkalosis of vomiting offset the chronic acidosis of renal failure = normal pH
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