Kedaruratan Metabolik

NURCAHAYA SINAGA
Metabolic
disturbance ?
Hypoglycemia
- A biochemical symptom,indicating the presence of an underlying cause
-Hypoglycemia is a common clinical problem in neonates, is less common
in infants and toddlers, and is rare in older childrenEpidemiology
Hypoglycemia is more common in
Etiology
neonates born at less than 37
- Hyperinsulinemia weeks' gestation and in those
- Metabolic defects born at more than 40 weeks'
- Disorders of glucose underproduction gestation, with incidence rates
- Toxins and other illnesses of 2.4% in neonates born at 37
- Large for gestational age in mother with type 1 weeks' gestation, 0.7% in
diabetes neonates born at 38-40 weeks'
gestation, and 1.6% and 1.8% in
neonates born at 41 weeks'
gestation and 42 weeks'
gestation, respectively
Symptoms of hypoglycemia in neonates include the
following:

Tremulousness, Brisk Moro reflex, Lethargy Poor feeding,

Irritability,Hypothermia Respiratory distress, Apnea, Bradycardia
Seizure, Coma, Sudden death

Symptoms of hypoglycemia in older children

include the following:
Dizziness, Sweating, Hunger, Anxiousness Confusion,
Lethargy, Poor feeding, Irritability
Seizure, Coma, Sudden death
Physical Examination :
Increased heart rate with bounding pulse due
to increased epinephrine secretion
Infants, if awake, may be irritable, tremulous, and cranky.
If the brain’s energy supply is severely impaired, the
patient's mental status is likely to be impaired, with
extreme inappropriate affect and mood, lethargy, seizure,
or coma
Differential Diagnoses
Pediatric Ethanol Toxicity Hyperinsulinism
Infant of Diabetic Mother Malnutrition
Maple Syrup Urine Disease (MSUD)
Oral Hypoglycemic Agent Toxicity
Panhypopituitarism
Pediatric Growth Hormone Deficiency Prematurity
Salicylate Toxicity
Workup
Approach Considerations
Plasma glucose concentrations should be
measured in all neonates and children with
the symptoms levels of more than 1.7
mmol/L/Newer publications suggest levels
of less than 2.5 mmol/L are inappropriate.
THE WHIPPEL TRIAD
1. the presence of symptoms likely or
known to be caused by hipoglikemia
2. a low plasma glucose concentration
when symptoms are present
3. subsequent relief of symptoms when
the hypoglycemia is corrected
- Short-term treatment of hypoglycemia consists of an
intravenous (IV) bolus of dextrose 10% 2.5 mL/kg.
-The critical sample should be drawn before the glucose is
administered.
- IV infusion that matches normal hepatic glucose production
(approximately 5-8 mg/kg/min in an infant and about 3-5
mg/kg/min in an older child
- Maintain the plasma glucose level at more than 3 mmol/L.
- Children with hyperinsulinemia may have much higher needs.
- Glucagon infusion at rates of 0.005-0.02 mg/kg/h should be used as

a temporary treatment in children with hyperinsulinism in whom

adequate amounts of dextrose cannot be given.
- It can cause a rash and decreased appetite if used over the
long term.
For hypoglycemia in patients with diabetes, treatment
depends on the patient's mental status :
If patient awake and alert
- 15 g of simple carbohydrate (4 oz of most fruit juices, 3
tsp of sugar, glucose tablets) by mouth should be
sufficient.
- Wait at least 15 minutes after the initial treatment
before retesting, because overtreatment of low blood sugar levels
in patients with diabetes is a common cause of hyperglycemia
If the patient's mental status is altered and aspiration
is a concern, treatment depends on the patient's setting
- At home, intramuscularly administered glucagon is the
best choice and should be available to families or close
associates of all insulin-treated patients with diabetes.
- In the hospital setting, IV dextrose 25% is
appropriate treatment
METABOLIC ACIDOSIS
arterial pH of less than 7.35 in the absence of an
elevated PaCO2
It is created by 1 of 3 mechanisms:
(1)increased production of acids,
(2)decreased excretion of acids, or
(3)loss of alkali.
The causes of a metabolic acidosis can be classified on the basis
of a normal or elevated anion gap.
Assessed in a complete investigation of the patient's history:
- Anorexia, nausea, vomiting, or diarrhea
- In pediatric patients, diarrhea
is the most common cause of a metabolic acidosis
- Metabolic acidosis associated with seizures, a depressed sensorium, or both in a
neonate
- This warrants consideration of an inborn error of
metabolism, or neonatal sepsis
- History of 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)
- Failure to thrive suggestive of chronic metabolic acidosis - This can be seen in
renal insufficiency or RTA
Assessed in a complete investigation of the patient's
history:
- New onset of polyuria, polydipsia, and weight loss - This
could signify undiagnosed diabetes mellitus and diabetic
ketoacidosis in a child
- Possible ingestion of a toxin or other form of intoxication.
Inquire as to what medications are in the home; suspect a
poisoning in a healthy child who quickly develops a metabolic
acidosis; possible agents are ethanol, ethylene glycol,
salicylates, and methanol
Hyperventilation or Kussmaul breathing may often be the first sign of a
metabolic acidosis in a child.
Breath sounds are often clear to auscultation (“quiet tachypnea”).
Patients with metabolic acidosis secondary to shock may have signs reflective of
single- or multiple-organ dysfunction, as follows:
- CNS manifestations may include lethargy, coma, and seizures
- Respiratory manifestations may include tachypnea, respiratory distress, and
hypoxemia
- Cardiovascular signs may include poor perfusion, weak pulses, tachycardia,
hypotension, murmurs, or a gallop
- Nonspecific abdominal symptoms and signs may be present such as
nausea, pain, vomiting, and altered appetite
- Signs of dehydration may include tachycardia, dry mucous membranes, and
- delayed capillary refill
Patients with diabetic ketoacidosis may present with fruity odor to their
breath
Approach Considerations :
An arterial blood gas
measurement reveals the
acidemia.
Bicarbonate Therapy
In instances in which the serum bicarbonate level is
only mildly to moderately depressed (>10-12 mEq/L),
bicarbonate replacement may not be necessary.
Emergent bicarbonate therapy may be warranted in
decompensated shock states in patients with a pH of
less than 7.15
The bicarbonate deficit can be calculated as follows:
(Desired Bicarbonate - Measured Bicarbonate) x
Weight (kg) x 0.6
Hyponatremia, defined as a serum sodium (Na)
concentration of less than 135 mEq/L, can lead
to hyponatremic encephalopathy, particularly in
prepubescent pediatric patients.
Serum sodium concentration and serum
osmolarity normally are
maintained under precise control by homeostatic
mechanisms involving stimulation of thirst,
secretion of antidiuretic hormone (ADH), and
renal handling of filtered sodium.
Hypervolemic hyponatremia
Total body sodium increases,
and TBW increases to a
greater extent. The ECF is
increased markedly, with the
presence of edema.
Redistributive hyponatremia
Water shifts from the
intracellular to the extracellular
compartment, with a resultant
dilution of sodium. The TBW
and total body sodium are
unchanged. This condition
occurs with hyperglycemia or
administration of mannitol.
Clinical presentation :
Patients with clinically significant hyponatremia
present with nonspecific symptoms attributable to cerebral
edema. These symptoms, especially when coupled with a recent
history of altered fluid balance, should suggest the possibility of
hyponatremia : Nausea and vomiting, Difficulty concentrating,
Confusion,Lethargy, Agitation,Headache,Seizures
Physical findings are highly variable and dependent on the degree and the
chronicity of hyponatremia.
Patients with acutely developing hyponatremia are typically symptomatic at a
level of approximately 120 mEq/L. Those patients with chronic hyponatremia
tolerate much lower levels. Most abnormal findings on physical examination are
characteristically neurologic in origin.
Level of alertness ranging from alert to comatose
Variable degrees of cognitive impairment (eg, difficulty with short-term recall;
loss of orientation to person, place, or time; frank confusion or depression)
Focal or generalized seizure activity
In those patients with acute severe hyponatremia, signs of brainstem
herniation, including coma; fixed, unilateral, dilated pupil; decorticate or
decerebrate posturing; sudden severe hypertension and respiratory arrest
Causes :
Hypovolemic hyponatremia develops as sodium and free water are lost and replaced
by inappropriately hypotonic fluids, such as tap water, half-normal saline, or
dextrose in water.
Sodium can be lost through renal or nonrenal routes.
Nonrenal routes include GI losses, excessive sweating, third spacing of fluids (eg,
ascites, peritonitis, pancreatitis, burns), and cerebral salt-wasting syndrome.
Excess fluid losses (eg, vomiting, diarrhea, excessive sweating, GI
fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily
by hypotonic fluids
Acute or chronic renal insufficiency, in which the patient may be unable to
excrete adequate amounts of free water
Salt-wasting nephropathy
Acute hyponatremia is less common than chronic hyponatremia and
typically is seen in patients with a history of sudden free water loading
(eg, patients with psychogenic polydipsia, infants fed tap water for 1-2
d, patients given hypotonic fluids in the postoperative period).
Acute evolution of hyponatremia leaves little opportunity for
compensatory extrusion of CNS intracellular solutes. The ultimate
danger for these patients is brainstem herniation when sodium
levels fall below 120 mEq/L.
The therapeutic goal is to increase the serum sodium level
rapidly by 4-6 mEq/L over the first 1-2 hours.
The source of free water must be identified and eliminated.
- Chronic hyponatremia must be managed with extreme care.
- Treatment of chronic hyponatremia has been associated with
the development of the osmotic demyelination syndrome (also
known as central pontine myelinolysis) characterized by focal
demyelination in the pons and extrapontine areas associated
with serious neurologic sequelae.
- Admit patients with severely symptomatic hyponatremia
manifested by coma, recurrent seizures, or evidence of brainstem
dysfunction to an ICU and monitor serum sodium levels closely.
Conclusion :
Metabolic :
hypoglycemia,
metabolic acidosis Looking for
and hyponatremia etiology
are not disease

Treatment
Need to base on
check
/laboratorium emergency
and etiology