Metabolic disorders

Chapter 27 Metabolic disorders



Diane King, Derek Louey



ELECTROLYTE EMERGENCIES



Theory



• Serum electrolyte concentrations are usually tightly controlled unless excessive gains or losses overwhelm homeostatic balance.

• Electrolyte balance requires normal hormonal control of intact kidney function. Primary renal dysfunction or the effects of drugs or endocrine disease can result in abnormalities.

• Water and electrolytes can be mobilised between plasma and other body compartments. This may occur under hormonal control.

• Serum electrolyte concentrations do not necessarily correlate with total body stores.


Causes/assessment



• Electrolyte losses: renal (drug effects or endocrinopathy), GIT (vomiting, diarrhoea, surgical drains), skin (sweating, burns)

• Electrolyte gains: ↓ renal elimination (renal failure, drug effects, endocrinopathy), GIT (diet, drugs), iatrogenic (intravenous therapy (IVT), total parenteral nutrition (TPN))

• Body compartment shifts: intracellular (e.g. potassium), bone (e.g. calcium, phosphate, magnesium)


Clinical effects



• Electrolytes have a role in establishing the membrane potential, receptor signalling and enzyme function.

• Depending on the electrolyte abnormality the central nervous system (CNS), cardiovascular system (CVS) and/or neuromuscular system can be affected.

• Clinical effect can vary from mild and non-specific to severe and life-threatening.

• Clinical impact is proportional to the severity and acuity of the derangement.

• If results are inconsistent with clinical information, repeat the test.


Management


Treat the patient, not just the abnormality.


• Mild cases—review and address causes, monitor abnormality.

• Moderate cases—as above plus begin treatment.

• Severe, life-threatening or resistant cases, e.g. neurological (seizures, coma), CVS (hypotension, abnormal ECG), respiratory muscle failure (hypoventilation, tetany)—get input from the intensive care unit (ICU).

Find and treat the cause, not just the abnormality. Often there is more than one mechanism operating, e.g. poor oral intake plus diuretic.


(See Table 27.3 for a list of electrolyte abnormalities, clinical indications and treatment.)



Table 27.3 Electrolyte emergencies (ICU involvement required)

image


ACID–BASE DISTURBANCES



Pearls/pitfalls



• An acute derangement in acid–base balance invariably signifies a significant disease process (most patients need admission or at least extended observation).

• An abnormal or recent change in venous bicarbonate may be the first clue to an acid–base disturbance.

• Arterial blood gas (ABG) determination is essential to fully categorise the disturbance, e.g. acidosis/alkalosis, respiratory/metabolic or mixed. Don’t just look at pH.

• Clinical information and other lab tests will help determine the cause.

• Treatment should primarily be directed at the cause of the disturbance and not by directly manipulating pH, e.g. sodium bicarbonate is indicated in only a limited number of causes of metabolic acidosis.


Normal values



• pH: 7.35–7.45

• pCO2: 35–45 mmHg (‘respiratory acid’)

• pO2: 100 mmHg

• [HCO3–]: 24 mmol/L (‘metabolic base’)


Determining the acid–base abnormality



1. Check pH: < 7.4 (acidaemic) or > 7.4 (alkalaemic)
• If acidaemic: is [HCO3–] < 24 (metabolic acidosis) or pCO2 > 40 (respiratory acidosis) or both?

• If alkalaemic: is [HCO3–] > 24 (metabolic alkalosis) or pCO2 < 40 (respiratory alkalosis) or both?

2. Is the respiratory compensation for a metabolic abnormality appropriate? (See ‘Metabolic equations’ in the ‘Quick reference’ section at the beginning of this book.)
• If pCO2 lower than expected: = concurrent respiratory alkalosis

• If pCO2 higher than expected: = concurrent respiratory acidosis

3. Is the metabolic compensation for a respiratory abnormality acute/incomplete or chronic/complete? (See ‘Metabolic equations’ in the ‘Quick reference’ section.)
• If [HCO3–] lower than expected: = concurrent metabolic acidosis

• If [HCO3–] higher than expected: = concurrent respiratory acidosis


Anion gap



• Anion gap approximates the unmeasured anions (usually [protein–], [SO42–], [PO43–]).

• Can be estimated as:


image



• Anion gap is diagnostically useful in metabolic acidosis (see below).

• A wide anion gap in the setting of metabolic alkalosis is suggestive of concurrent metabolic acidosis.


Metabolic acidosis


(Mild: [HCO3–] < 18 mmol/L; moderate: < 15 mmol/L; severe: < 12 mmol/L)


This is the commonest metabolic abnormality seen in the emergency department. Frequently under-recognised and under-treated (low venous HCO3– on serum electrolytes is the first clue). pH may be (temporarily) near normal if well compensated.


• Important causes of wide anion gap metabolic acidosis: poor tissue perfusion, hypovolaemia and/or sepsis (most common), diabetic ketoacidosis (DKA), renal failure, drug poisoning.

• Rare but important causes: thiamine deficiency, metformin.

• Less common causes: bicarbonate loss from GUS or GIT/‘normal anion gap metabolic acidosis’ e.g. renal tubular acidosis, surgical fistula/stomal/drain losses, Addison’s disease.

• Rapidly assess the following—circulatory status (HR, BP, urine output), infection (fever), hyperglycaemia (bedside blood sugar level (BSL), urinary ketones).

• Important lab tests—electrolytes, anion gap, renal function, serum osmolarity, serum ketones, BSL, WCC.


Management



1. Treat cause:
• hypovolaemia—fluid challenge until vital signs and urine output restored

• sepsis—fluid challenge, early administration of antibiotics

• DKA—see Chapter 26, ‘Endocrine emergencies’

• renal failure—see below

• poisoning—obtain toxicology advice

• normal anion gap acidosis—bicarbonate infusion.

2. Potassium deficit may be unmasked as the metabolic acidosis resolves. Begin replacement if already hypokalaemic or when adequate urine output established (see ‘Management’ under ‘Hyperkalaemia’).


Metabolic alkalosis


(Mild: [HCO3–] > 25 mmol/L; moderate: > 30 mmol/L; severe: > 35 mmol/L)


• Common causes in emergency department include: diuretic use, gastric losses (e.g. pyloric stenosis, bulimia nervosa).

• Less common causes: excessive corticosteroids (Cushing’s syndrome, hyperaldosteronism).

• Perpetuating factors: dehydration, hypokalaemia.


Management



1. Most are ‘saline (chloride) responsive’ (urine [Cl–] < 25 mmol/L)—correct dehydration with normal saline (contraindicated in oedematous states).

2. Potassium depletion needs to be corrected (see ‘Hypokalaemia’).

3. Stop offending medications.

4. Treat cause.

5. If ‘saline unresponsive’ [urine [Cl–] > 40 mmol/L], may need HCL via central venous catheter (CVC) (manage in ICU).


Respiratory acidosis


(Mild: pCO2 > 45 mmHg; moderate: > 55 mmHg; severe > 65 mmHg)


• Any cause of respiratory depression or inadequate alveolar ventilation.

• Common emergency department causes include: acute cardiorespiratory illness (asthma/COAD, pulmonary oedema, pneumonia), CNS insults (opiates, benzodiazepines, acute space-occupying lesion), trauma (head injury, flail chest, haemo/pneumothorax).


Management



1. Treat cause.

2. Mechanical ventilation (especially if drowsy/somnolent, severe head injury).

3. Common mistake—decreasing fraction of inspired oxygen (FiO2

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Jun 14, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Metabolic disorders

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